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The definition of glaucoma has evolved in the recent decades to include more than simply "increased intraocular pressure." In the most recent edition of Veterinary Ophthalmology , glaucoma was defined as "the final common pathway of a group of diseases with decreased retinal ganglion cell sensitivity and function, retinal ganglion cell death, optic nerve axonal loss and concurrent optic nerve head enlargement, incremental reduction in visual fields, and blindness. Most of these diseases in the dog either result in or are associated with increased intraocular pressure in their mid to late stages." Although this definition is complicated, it does serve to highlight the fact that our understanding of the various clinical manifestations of the disease syndrome "glaucoma" is expanding. The most clinically tangible aspect of this disease remains to be increased intraocular pressure (IOP).
Primary glaucoma is characterized by elevated intraocular pressure in the absence of signs of concurrent ocular disease. Most dogs with primary glaucoma suffer from narrow angle glaucoma, in which the iridocorneal angle progressively closes over time, resulting in obstruction of aqueous outflow through the iridocorneal angle (figure 1). Primary open angle glaucoma is the most common form of glaucoma in people and is characterized by a more chronic insidious onset. In the canine population, open angle glaucoma exists almost solely in the Beagle. Unfortunately, primary glaucoma (either narrow angle or primary open angle) is a bilateral disease, with the fellow eye being affected within 6 to 12 months of initial diagnosis. Client education regarding the eventual prognosis is therefore a crucial part of the clinical management of primary glaucoma. It is also important to educate clients regarding the heritability of primary glaucoma and to discourage breeding of affected dogs. Prophylactic therapy of the fellow eye has been shown to increase the time to onset of glaucoma, but not to prevent glaucoma altogether. Secondary glaucoma is characterized by elevated intraocular pressure associated with concurrent ocular disease. The most commonly associated ocular diseases include uveitis, intraocular hemorrhage, neoplasia, and lens displacement (Figure 2). Uveitis, depending upon its cause, can be unilateral or bilateral. In uveitis, inflammatory mediators are liberated into the eye and result in changes in the iridocorneal angle. Pre-iridial fibrovascular membranes and inflammatory cells cause obstruction of the angle, impeding aqueous egress. Peripheral anterior synechiae may also block the angle. Treatment is directed towards controlling inflammation with topical steroids and atropine. Intraocular hemorrhage is similarly managed. Glaucoma secondary to intraocular neoplasia carries a grave prognosis for saving the eye due to relatively limited options of successfully treating intraocular tumors. Lens luxation, although classically considered a form of secondary glaucoma, has many of the characteristics of primary glaucoma. Since there is a breed predisposition for lens luxation, glaucoma secondary to lens luxation is also considered a bilateral disease. Although the best chance of saving vision and preventing glaucoma is by removing the lens, glaucoma may still develop or persist after surgery.
The clinical signs of glaucoma vary greatly by stage. In early glaucoma, episcleral venous congestion and conjunctival hyperemia are present, resulting in a "red" eye (Figure 3). The eye is painful! Depending upon the severity of the pressure rise, vision may or may not be present. The pupil may be normal or slightly dilated in room light (Figure 4). Pupillary light reflexes are sluggish to normal. Mild corneal edema is also often present. At this stage, tonometry is invaluable! There is no clinically reliable way of distinguishing glaucoma form the other causes of "red eye" without measuring the intraocular pressure. Because eyes with early glaucoma are often still visual or have the potential for vision, it is crucial to identify these cases early and to treat them aggressively. The clinical signs of late glaucoma include buphthalmos, corneal striae, optic disc cupping, and retinal degeneration (Figure 5). These eyes may also exhibit exposure keratitis and lens luxation. Although buphthalmos is easily recognizable and pathognomonic for glaucoma, by the time an eye is buphthalmic, it is blind. This is not always true in puppies: their collagen is able to stretch and deform more easily. Once the intraocular pressure in a puppy is controlled, vision may return and the globe may return to a more normal size.
The
goals of medical management of glaucoma include the reduction of intraocular
pressure, improvement of blood flow to the optic nerve and retina, and
decreasing the damage caused by toxic metabolites such as glutamate (Figure
6).
Osmotic agents, such as mannitol and glycerol, are used in the emergency
management of glaucoma to rapidly decrease IOP. Carbonic anhydrase inhibitors
(CAI) can be administered orally or topically to effectively decrease
aqueous production. Oral admainistration of CAIs can be associated with
side effects such as hypokalemia, anorexia, vomiting, diarrhea, metabolic
acidosis, lethargy, and depression. Miotic agents (pilocarpine, demarcarium
bromide) increase aqueous outflow but may potentiate uveitis, and therefore,
must be used with caution in eyes with significant intraocular inflammation.
Beta-blockers, such timolol maleate, are the most common glaucoma medications
in people. Research has shown that significantly higher concentrations
of timolol than are commercially available are needed to reduce IOP in
dogs, however. Despite this fact, timolol is commonly used to treat glaucoma
in canine patients. Sympathomimetic agents, such as epinephrine and dipivefrin,
are used to increase aqueous outflow. The most recent addition to the
armamentarium of glaucoma drugs is Xalatan® (Pharmacia Upjohn), a
synthetic topical prostaglandin analogue that increases unconventional
(uveoscleral) aqueous outflow. It
is important to note that medical therapy of glaucoma is almost always
results in eventual progression of the disease. Multiple drug therapy
is often required to adequately control IOP. Frequent monitoring of IOP
by tonometry is essential in adequately monitoring therapy. Clients should
be advised of the poor long term prognosis of this disease in order to
avoid dissatisfaction. They should also be instructed to carefully monitor
the fellow eye for early signs of glaucoma: namely, mild increases in
redness, ocular discomfort, cloudiness of the eye, or discharge. Client
education is a cornerstone of the clinical management of glaucoma!
Surgical
therapy is adjusted accordingly to the visual status of the patient. In
visual or potentially visual eyes, cyclodestructive or filtering procedures
are considered. In irreversibly blind, painful, glaucomatous eyes, salvage
procedures are recommended to alleviate pain. The most common salvage
procedures include enucleation, intraocular silicone prosthesis (ISP)
placement, and chemical cycloablation by intravitreal injection of gentamicin.
The
surgical technique of ISP placement is straightforward and will be presented.
A few special instruments greatly facilitate the surgery: Jameson caliper
(Figure
11),
Carter sphere introducer (Figure
12),
cyclodialysis spatula (Figure
13),
and lens loop (Figure
14).
Silicone prostheses are available in a variety of sizes. In small animal
patients, the size of the prosthesis to be placed is determined by measuring
the horizontal corneal diameter of the "good" eye with the Jameson
caliper and adding an additional 1 - 2 mm. For example, if the horizontal
corneal diameter of the "good" eye is 16 mm, then the most appropriate
size for the ISP is most likely 17 or 18 mm in diameter.
The
complication rate with ISP surgery is slightly higher (9.1% - 16%) than
that seen with enucleation (estimated at less than 3%). Potential complications
include ulcerative keratitis, rejection of the prosthesis, dehiscence
of the scleral suture line, endophthalmitis/ panophthalmitis, and regrowth
of undiagnosed tumors. By emphasizing proper patient selection for ISP
placement, one author estimated the overall complication rate could be
as low as 4%. As
with many surgeries, patient selection for ISP placement is important.
Eyes with keratoconjunctivitis sicca (KCS) may not heal well after the
surgery or may be prone to corneal ulceration due to tear film abnormalities.
Eyelid abnormalities such as entropion or eyelid tumors may need to be
corrected before surgery in order to avoid post-operative irritation of
the cornea. Eyes with active corneal ulceration at the time of surgery
are to be avoided since the ulcer may not heal well after the cornea has
been stressed by surgery. Eyes with infectious endophthalmitis are at
greater risk of dehiscence and ongoing endopthalmitis/ panopthalmitis.
The subject of ISP surgery in cases of intraocular neoplasia is controversial:
many authors believe ISP placement in these eyes is contraindicated. There
are others, however, that assert that since many intraocular tumors are
benign, placement of the ISP does not necessarily incur any problems.
If the tumor recurs after evisceration, the globe may need to be enucleated
at that time. By taking these factors into account, post-operative complication
with intraocular silicone prostheses can be minimized.
The
post-operative care of a patient with an ISP is also important, and slightly
different for patients that have undergone the other salvage techniques
of enucleation or intravitreal gentamicin injection. Post-operative pain
is subjectively greater in ISP patients and therefore the use of appropriate
analgesics is important. Moderate to severe periorbital swelling is common
in the immediate post-operative period. This swelling can be minimized
with perioperative non-steroidal anti-inflammatory medications such as
carprofen or ketoprofen. Although the majority of the swelling resolves
within the first week post-operatively, the conjunctiva may remain swollen
and hyperemic for as long as one month. As the blood remaining within
the globe resolves over time, it may take on a greenish hue due to the
normal breakdown products of hemoglobin. This is normal and is not cause
for concern. Topical antibiotic ointments are used three to four times
a day for the first post-operative month. Fluorescein stain should be
performed weekly in the first month as well (Figure
15), (Figure 16), (Figure 17), (Figure 18).
Elizabethan collars can be used to minimize self-trauma after surgery.
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