# Aqueous Humor Dynamics

Rate of fluid production = rate of fluid outflow or drainage (faucet and drain analogy)
There is some resistance to fluid outflow at the iridocorneal angle; otherwise, the anterior chamber would collapse.
This resistance to outflow results in an intraocular pressure of approximately 8-18 mmHg (will vary somewhat depending on what instrument is used to measure IOP).
In accordance with Pascal’s law, IOP is equal throughout eye (i.e., if IOP = 23 mmHg in anterior chamber, it’s also 23 mmHg in posterior chamber and vitreous cavity).

# “Conventional” or “Trabecular” Outflow

Nonpigmented epithelium of ciliary body
Posterior chamber
Through pupil
Anterior chamber
Iridocorneal angle
1. Pectinate ligaments
2. Trabecular Meshwork
Intrascleral venous plexus
Systemic circulation

# “Unconventional” or “Uveoscleral” Outflow

Nonpigmented epithelium of ciliary body
Absorption directly into uveal tissue
Supraciliary space
Sclera
Systemic circulation

# Definition of Glaucoma

A group of diseases characterized by increased IOP, resulting in damage to the ganglion cells / optic nerve. While we are going to talk a lot about the cause of elevated IOP and ways to reduce it, I want you to think of glaucoma, first and foremost, as a disease of the optic nerve because it’s the optic nerve damage that results in blindness.

# Classification of Glaucoma

Glaucoma can be classified in three ways:

Depending on whether the glaucoma is a primary or secondary problem
On the status of the iridocorneal angle
On the duration of the glaucoma (i.e., acute vs. chronic)

Each specific case should be classified on the basis of all three when possible….e.g., one could say that a given glaucoma case is an acute case of primary glaucoma with a dysgenetic angle (i.e., goniodysgenesis).

The status of the angle is important because elevated IOP always due to decreased aqueous humor outflow. While it would be logical to theorize that glaucoma could also occur due to increased production of aqueous humor, we don’t think this ever really occurs clinically

Angles are described by their morphologic appearance, which often correlates with how well they function….i.e., a more open angle will drain fluid more efficiently than a less open angle. But be aware that this is not always the case; for example, there is a type of glaucoma called Primary Open Angle Glaucoma (POAG) in which the angle is morphologically perfectly normal, but fluid outflow is still severely impeded because of a physiologic, not morphologic, dysfunction.

Open angle – the angle, as judged in degrees, is wide open. Usually appears to be approximately 40o or so between the cornea and iris. In addition, this description implies that the pectinate ligaments are properly formed.
Narrow angle – the angle is narrower than normal as a result of anterior displacement of the iris. Can occur as a primary problem with the iris, or due to the iris being pushed anteriorly by an enlarged lens. The angle also narrows with progression of goniodysgenetic glaucoma (see below).
Closed angle – the peripheral iris is in contact with the peripheral corneal endothelium, effectively obliterating the angle. Permanent adhesion between the peripheral iris and peripheral cornea is termed “peripheral anterior synechia” (PAS). The angle can close as a result of the progression of goniodysgenesis or as a feature of just about anything that causes secondary glaucoma (see below).
Goniodysgenesis – This is a congenital angle defect we’ll discuss below. Hard to know where to put it in this scheme. Some people keep it out as a separate category (ie., a dog’s angle can be open, narrow, closed or dysgenetic) while other folks consider it a form of closed angle. Might be easier on your brains to consider it as a separate form of angle abnormality because dogs with dysgenesis can go on to narrow and/or close their angles in the more “traditional” sense as described above.

# Primary Glaucomas

Goniodysgenesis (also called pectinate ligament dysplasia): a solid sheet of tissue (usually with a few “flow holes”) is present in place of pectinate ligaments. Aqueous cannot exit through this separate sheet of tissue rapidly enough, so if aqueous production stays constant IOP will rise. Your text separates goniodysgenesis out as a cause of a separate category of glaucoma, congenital glaucoma. I think that’s misleading because while the angle abnormality is congenital, the glaucoma develops later in life. Breeds commonly afflicted with primary glaucoma include cocker spaniel, chow, siberian husky, sharpei, and bassett hound. I suggest thinking of goniodysgenesis as a type of closed angle (again, some separate goniodysgenesis from closed angles). Hence, dogs with glaucoma and goniodysgenesis have primary angle closure glaucoma (PACG).
Narrow angle glaucoma: angle (in degrees) formed between iris and cornea progressively decreases with age. This results in more resistance to outflow than normal, and therefore raises IOP. As IOP increases, angle narrows further, and may eventually collapse causing a sudden and dramatic spike in pressure. In dogs with goniodysgenesis, the angle often narrows as IOP increases. In my opinion a narrow angle alone (without predisposing goniodysgenesis) does not raise IOP in dogs.
Open angle glaucoma: the angle is morphologically normal, but there is a functional retardation in the transmission of aqueous from the trabecular meshwork into the intrascleral venous plexus. This is far and away the most common cause of glaucoma in humans, but essentially never happens in dogs. This glaucoma is usually referred to as POAG (primary open angle glaucoma).
Primary glaucomas have strong breed predilections and are essentially always bilateral, although the IOP elevation in the two eyes generally doesn’t occur at exactly the same time (may be months to years between first eye and second eye).

# Secondary Glaucomas

Uveitis
Anterior lens luxation
Hyphema
Intraocular tumors
Pigmentary glaucoma of Westies
Pigmentary glaucoma of Golden Retriever
Most of the secondary glaucomas can be unilateral or bilateral. The pigmentary glaucomas, however, are almost always secondary.

# Duration of disease

The length of time that the IOP elevation has been present is an important part of the classification scheme because it is the single most important determinant of therapy. We will cover this in detail later, but the general concept is that animals with glaucoma need treatment for two reasons: glaucoma is blinding, and glaucoma hurts.
The blindness is due to retinal ganglion cell damage (which is equivalent to saying optic nerve damage….it should be clear to you why these are equivalent statements), and this damage becomes permanent within hours to days depending on how high the IOP is.
If you think duration is relatively short (say, a few weeks at most, but preferably less than one day) you should be therapeutically aggressive in an effort to salvage vision.
But if the duration is more chronic, a completely different set of “salvage” options (such as enucleation) become viable to simply alleviate the discomfort.
The disappointing, unvarnished truth is that the vast majority of both primary and secondary glaucomas are already relatively chronic by the time the animal’s guardian knows there’s a problem, so retention of vision is relatively uncommon. We will talk about how to differentiate chronic from acute later.

# Diagnostic Techniques

# Tonometry

There are three types of tonometers in common use in veterinary clinics at present:

Applanation tonometers: Most common example is the TonoPen™ (or it’s more recent incarnation, the TonoPen Avia™).

Principle: the circular tip of the instrument has a defined surface area. It is advanced towards the cornea and pressed until the instrument senses that the cornea has been flattened (or “applanated”) by that same surface area. A transducer in the handpiece then measures how hard you’ve had to push to flatten the cornea by that amount, and then calculates the pressure in the eye that must have been pushing back against you (i.e., the IOP). Very easy to use, very reliable. Can be a bit persnickety until you get the hang of it. Pretty expensive (in the $1800 - $4000 range depending on model and new vs. used). Requires topical anesthetic.
Rebound tonometer: Most common example is the TonoVet™.

Principle: a little probe with a round plastic tip is thrown at the cornea, and the probe then rebounds off the cornea back into the instrument. The instrument measures the speed of the rebound, and calculates IOP from that speed. Does not require topical anesthetic, and fractious animals tend to object less to this instrument than to the TonoPen. Only disadvantage is that it must be held with probe parallel to the floor. Generally felt to be more accurate than the TonoPen, but in my view the difference is negligible. Cost is around $3500.
Indentation tonometer: Most common example is the Schiotz tonometer.

Principle: A known weight is placed on the surface of the cornea (the “base” weight is 5.5 gm). The distance that this weight can indent the cornea is measured. The IOP is determined from a table of values of indentation distance vs. IOP. If indentation distance is 0, a weight is added to give more chance of providing some degree of indentation. To use the Schiotz the dog must be sitting down and looking straight up, and requires topical anesthetic. Definitely the least convenient of the three methods, but not really that bad once you get used to it. Costs in the $200 - $500 range.

A few things to bear in mind about tonometry

First, there is no single number that is “normal.” Rather, we have the concept of a normal range, which will vary a little depending on which tonometer you use. Let’s go with a range of 8-18 mmHg as being “normal,” knowing that any individual reading may be normal or abnormal for a given dog depending on other clinical signs.
Second, none of these tonometers actually measures IOP….rather, they all estimate IOP. Because they all make these estimates by different methods, they will usually give slightly different results. But they are all close enough for our purposes to be considered equivalent.
Third, your text implies that the Schiotz is unacceptable for veterinary ophthalmology……HOGWASH! This is a great instrument, and is far more affordable than the others. However, because of the inconvenience associated with its use most veterinarians prefer the TonoPen or TonoVet.
Fourth, your text mentions a few other tonometers……pneumotonometer, Goldmann tonometer, eye puff tonometer…we’re not going to include these in our discussions. Veterinary ophthalmologists don’t use these instruments routinely.

# Gonioscopy

Direct visualization of the canine iridocorneal angle isn’t possible because the geometry of the cornea doesn’t allow light reflected off the angle to exit the eye. Rather, is it completely reflected back into the eyeball. In gonioscopy a large silicone or plastic lens is placed on the cornea to get around this problem. Visualization of the angle allows for detection of goniodysgenesis, PAS, angle tumors, etc. This assessment can often have prognostic value. In all honesty, this technique is as much art as science, and as such GPs don’t do it enough to make it worth their while. It is pretty much relegated to the ophthalmologist.

# Ophthalmoscopy

The appearance of the retina and optic nerve is prognostically important. Optic disc cupping is when the disc of a glaucoma patient is depressed caudally due to elevated IOP and compression of the lamina cribrosa (if you don’t recall the lamina, please review notes from the anatomy lab). Cupping generally implies at least some degree of chronicity. With even more chronicity the nerve actually becomes atrophic, in which the nerve head appears small, dark, and scalloped. In addition, chronic cases may have wedge-shaped areas of hyperreflectivity called “watershed” lesions which may represent ischemia of short ciliary arteries.

# High resolution ultrasound

High resolution ultrasound of the angle, tonography, and provocative testing (either water or steroid provocation) are all informative but aren’t routinely pursued clinically.

# Clinical and Pathologic Effects of Elevated IOP

Make note of which clinical signs are only seen with chronicity

Vision
Can be blind or visual, depending on how high the pressure is and how sensitive the individual’s optic nerve is. If blind, vision may or may not be restorable, with the primary determinant of vision being how chronic the IOP elevation is.

Retina and optic nerve
Glaucoma destroys retinal ganglion cells and optic nerve; mechanism probably combination of vascular and mechanical. Elevated IOP eventually affects all parts of the eye, but these inner retinal elements are the most sensitive. Clinically, these changes are eventually manifested as optic disc cupping and optic nerve atrophy; you generally won’t see cupping or atrophy until the case is somewhat chronic. With high enough IOPs and enough chronicity, outer retinal elements also become affected.

Among the things that bite about having a patient with glaucoma, perhaps the worst is that in many cases (in fact, probably most cases) once optic nerve degeneration has commenced it can continue unabated even if IOP is successfully returned to normal.
Hence, in the future major therapeutic efforts will go beyond simply normalizing IOP and will include some sort of therapy aimed specifically at protecting the optic nerve as well……see “Neuroprotective Therapy” below.

Cornea
Edema of the stroma; pressure induced damage to endothelial cells and hydrostatic forcing of aqueous into cornea both contribute to edema. With buphthalmia (see below), Haab’s striae (i.e., break’s in descemet’s membrane) and exposure keratitis associated with lagophthalmia…thus, Haab’s striae and exposure keratitis are associated with chronicity.

Ciliary body
Ciliary body destruction occurs with chronicity, resulting in reduced aqueous formation and reduction of IOP.

Pupil
Mydriasis due to ischemic necrosis of the iris sphincter muscle

Globe and fibrous tunic
Buphthalmia (i.e., enlargement of the globe); sclera stretches and thins in response to the increased pressure. This is a sign of chronicity, and by the time the globe is enlarged you can be about 99% certain that the optic nerve is already toast by the time buphthalmia occurs. Also injection of episcleral vasculature as increased pressure inside eye shunts venous return to more superficial episcleral vessels.

Lens
Subluxation due to ciliary zonules rupture secondary to buphthalmia (therefore this is also a sign of chronicity). Beware: while glaucoma can cause luxation, luxation can also cause glaucoma. We will discuss how to differentiate when we discuss lens disease.

Aqueous humor
Will occasionally see flare, probably due to pressure-induced damage to the blood aqueous barrier. Note that this is an exception to the maxim that flare is pathognomonic for anterior uveitis

Iridocorneal angle
In dogs with goniodysgenesis angle will gradually narrow and close with chronicity. Unfortunately you’re not really going to know this is occurring because it’s unlikely gonioscopy will be part of your ocular diagnostic arsenal, but it’s not going to change your therapeutic approach anyway.

Pain
Ocular and/or systemic. Recent information suggests that pain is not so much associated with any particular IOP, but rather with how quickly IOP rises.

# Primary Glaucoma

The section on primary glaucoma in your text is, in my opinion, unnecessarily confusing. Don’t get bogged down on the details of the Zurich study vs. the Utrecht study, etc.

# Goniodysgenesis

Your text also refers to this condition as pectinate ligament dysplasia, and you can treat these as synonymous terms. There is a strong breed predisposition for goniodysgenesis, with Bassets, Cockers, Chows, Bostons, Huskies, Akitas, Danes and Shar Peis being the most common offenders. However, any breed, and even mixed breeds, can be affected with goniodysgenesis. There is a female predilection for goniodysgenesis, and most dogs are in the 4-8 yr. range when initially diagnosed (although I have seen dogs in their teens when first diagnosed). In utero, all dogs have a solid sheet of tissue in the plane of the adult pectinates. Beginning about 2 weeks prepartum, and continuing up until about 2 weeks postpartum, this sheet of tissue undergoes a process of rarefaction in which the only tissue left behind are the pectinates. In goniodysgenesis, this rarefaction process is aborted, leaving the sheet of tissue (usually with attempts at flow hole formation) where the pectinates should have been. It is strongly suspected that goniodysgenesis is inherited, although the mode of inheritance has not been identified nor has any causative gene. In the early stages of PACG due to goniodysgenesis, the clinical signs are subtle and may be limited to mild hyperemia and perhaps mild corneal edema. Even if these dogs are lucky enough to be presented to a veterinarian at this stage, it is often the case that IOPs are not measured at this juncture thus missing a potential opportunity to extend the time of useful vision….thus, it is imperative that every dog who presents to you with a red, cloudy eye must have IOP measured! With persistence of high IOP, and possibly due to idiopathic intermittent higher spikes of IOP, episcleral injection and severe edema with blindness ensues. In the vast majority of cases, by the time these cases present to the veterinarian it is too late to restore vision.

# Narrow angle glaucoma

Indicates that the angle in degrees between the iris and the cornea is less than normal, and it is logical that such a situation would retard outflow and raise IOP. Although debatable, I don’t believe narrow angle glaucoma really occurs as a primary glaucoma syndrome in dogs. When we see narrow angles I feel that they represent a secondary progression of goniodysgenetic angles.

# Open angle glaucoma

The angle is morphologically normal, but there is functional retardation of outflow at the level of the intrascleral venous plexus (we think). Not really seen clinically in dogs with any degree of regularity. When it does occur, it’s almost exclusively seen in the beagle, and beagles in purpose-bred experimental colonies at that. POAG in beagles is inherited as an autosomal recessive trait, and is due to a mutation on a gene called ADAMTS10.

# Primary glaucoma and breed

The many pages in your text devoted to individual breeds and primary glaucoma can be summed as follows: primary glaucomas in most breeds are associated with some degree of goniodysgenesis. It is true that many dogs can have variable degrees of goniodysgenesis and never suffer from elevated IOP, but most dogs with primary glaucoma have large areas of goniodysgenesis. The “poster child” breeds for glaucoma due to goniodysgenesis are the Basset Hound, Cocker Spaniel, Boston Terrier, Chow, and Siberian Husky. POAG is pretty much limited to the Beagle, and even there it’s pretty much exclusively found in purpose bred research colonies (i.e., you’re not going to see these in clinical practice).

# Secondary Glaucoma

Secondary glaucoma is elevation in IOP associated with some other primary condition that obstructs aqueous outflow. For example, in dogs with chronic uveitis, inflammatory debris and fibrovascular membranes both obstruct the angle leading to elevated IOP. Obviously, in addition to aiming treatments at reducing IOP, efforts must be made to alleviate whatever the primary cause is.

# Causes of secondary glaucoma

# Uveitis

Anterior uveal inflammation can cause retardation of aqueous outflow by several mechanisms.

You should be familiar with causes of uveitis from the first part of the course.
Peripheral anterior synechia (PAS) – Peripheral iris adheres to peripheral corneal, thus obliterating the iridocorneal angle and resulting in decreased outflow. Such angles are, then, by definition closed angles.
Iris bombé - Syndrome of 360o posterior synechiae of the pupil to the lens. Aqueous from ciliary body builds up in posterior chamber because it can’t get through pupil. Peripheral iris then balloons forward and angle collapses, resulting in PAS and IOP elevation. Again, these are closed angles.
Clogging of pectinates and trabecular meshwork with inflammatory cells and inflammatory debris
Formation of preiridial fibrovascular membranes (PIFMs) – can grow across pupil, causing “pupillary block” and also across angle retarding outflow.

# Lens luxation

Lens luxation means displacement of lens associated with breakage of lens zonules
Luxations are classified by relationship of lens to iris: lens in front of iris, anterior luxation; lens behind iris, posterior luxation.
Subluxation: lens zonules are partially disrupted so lens is loose but not completely out of position
If lens luxates into the anterior chamber (and on occasion even if it stays posterior to the iris) it can occlude the angle and cause IOP elevation.
Lens luxation can cause glaucoma (this would be primary luxation with secondary glaucoma), but lens luxation can also be caused by glaucoma (in which case the luxation would be secondary; the glaucoma in these circumstances can be primary or secondary). So how do you tell which came first?
- It’s not always easy!
- In general, if luxation is primary it’s usually in a predisposed breed (typically terriers, esp. Jack Russell) and luxation is anterior
- If luxation is secondary to glaucoma, it occurs because the zonules break as a result of stretching in association with buphthalmia (i.e., if the globe isn’t buphthalmic, the luxation isn’t secondary)
- In general, when the glaucoma is secondary to luxation the luxation is posterior and is generally actually a subluxation.
- Understand that it is possible to have a luxation that is secondary to a secondary glaucoma….for example, severe uveitis → synechiae, PIFMs, bombe, etc → IOP elevates (i.e., secondary glaucoma) → with chronicity, globe becomes buphthalmic → zonules break → luxation.
- It has recently been suggested that the same gene that codes for primary lens lux also can code (in some circumstances) for POAG….well, that bites, because then even appropriate treatment of the primary lux doesn’t guarantee that glaucoma won’t occur anyway. So here’s a situation in which both the lens lux and the glaucoma are primary!
Lenses can luxate for reasons other than primary and secondary to glaucoma….we’ll talk more about these (as well as lens lux therapy) in the lecture on lens disease.

# Aphakic/Pseudophakic glaucoma

Glaucoma secondary to cataract surgery
- Note that not every post-cataract surgery IOP elevation is glaucoma per se; some are simply postoperative ocular hypertension (see below)
Easily the most common cataract surgery complication (reports of up to 15% of cataract surgery cases)
Pathogenesis unclear. Probably involves postoperative uveitis, with various degrees of pupil block, PIFM formation, inflammatory debris, etc.
Breed predispositions: Bostons, Cockers, Shih Tzus; unclear why these breeds develop glaucoma after cataract surgery more than others.

# Post-cataract surgery ocular hypertension

Differentiated from aphakic/pseudophakic glaucoma because it is a transient rise that occurs in the immediate postoperative period
It is unknown whether or not this transient IOP rise is enough to damage the optic nerve, and it is also unclear whether or not dogs with postop ocular hypertension are at risk to become “aphakic/pseudophakic glaucoma” dogs later down the road.
Can occur anytime in the first 24 hrs post op, but most will occur 4-8 hours postop.

# Hyphema

Blood in the anterior chamber
Common causes: retinal detachment, chronic uveitis, clotting disorders, trauma, intraocular tumors
Erythrocytes and macrophages laden with erythrocytes clog angle

# Intraocular tumors

Tumor itself can clog angle
Also, intraocular tumors can spontaneously bleed (see hyphema above)

# Melanocytic glaucoma of Cairn Terriers (aka pigmentary glaucoma of CT)

Idiopathic accumulation of melanocytes/melanophages in sclera and angle
Obstructs outflow
Chronic, smoldering IOP elevation
Exceedingly difficult to treat successfully

# Pigmentary glaucoma of Golden Retrievers

Begins as an idiopathic accumulation of pigment, usually in a spokelike fashion on the anterior lens capsule
Most cases have iris cysts, which can be confusing because lots of Goldens have perfectly benign cysts
Also includes idiopathic accumulation of proteinaceous debris on lens capsule and in the anterior chamber – therefore these dogs sometimes have flare. Some ophthalmologists (myself included) think this material may be exuding from the cysts.
This was initially thought to be a uveitic syndrome because the proteinaceous debris causes flare.
As with the Cairn Terrier syndrome, treatment is frustrating and usually unsuccessful

# Other comments:

Most of the secondary glaucomas can be unilateral or bilateral. The pigmentary glaucomas, however, are almost often bilateral.

Secondary glaucomas are generally more difficult to bring under control than primary glaucomas (not that the primaries are easy to treat either!).

# Therapy

Glaucoma does two bad things: (1) it causes blindness, and (2) it hurts. So the first order of business with a glaucomatous dog is to determine your goal: restoring/preserving vision vs. making dog comfortable.

Remember that the primary focus of glaucoma therapy is lowering IOP. All IOP-lowering therapies must either reduce aqueous production or increase aqueous outflow.
Can vision be restored?
- Is vision currently present?
- How long has pressure been elevated? Signs of chronicity? Buphthalmia? Posterior lens subluxation? Optic disc cupping or optic nerve atrophy?
- Glaucoma can cause irreversible vision loss in a matter of days, depending on the severity of IOP elevation.

If goal is maintaining vision, treat as an emergency!

# Emergency therapy

Prostanoid eye drops

The mechanism of action of these agents in dogs is unknown, but probably includes reduction of aqueous production AND increase of both trabecular and uveoscleral outflow.
A very potent IOP-lowering class of drugs in dogs
Rapid acting. Demonstrable effect within 1-2 hrs.
Latanoprost, bimatoprost, travaprost

Carbonic anhydrase inhibitors

The following reaction occurs in the ciliary nonpigmented epithelium and is important in the production of aqueous humor:

H₂O + CO₂ ←→ H₂CO₃ ←→ HCO₃^- + H⁺
Both reactions are catalyzed by carbonic anhydrase, so inhibition of CA results in reduced aqueous production.

The primary topical CAI is dorzolamide

Very potent, although probably a notch behind prostanoids in this regard
Takes effect within 1-2 hrs
Stings a bit on instillation

Also available as orals

Methazolamide, dichlorphenamide
Lots of side effects when administered systemically
These days we generally use a combination product that contains both dorzolamide and the β–blocker timolol (see below). Of the two agents in this product, the dorzolamide is doing most of the work The proprietary name of this produce tis CoSopt.

Osmotic diuretics

Mannitol, 1 gm/# slowly IV (over 30-60 minutes)
Withhold oral water for 2 hours.
Works by dehydrating eye and reducing ocular volume. Rapid onset (30 minutes), short duration (6 hours), and very potent

If emergency medical therapy fails, surgery may be needed on an emergency basis. Surgical procedures are described below with maintenance medical therapy

Once IOP is reduced, commence maintenance therapy to keep IOP down

If IOP elevation is secondary to anterior lens luxation, emergency lens removal is indicated.

# Maintenace medical therapy

Latanoprost (or other prostanoid). Usually a BID therapy
CoSopt. Usually a BID therapy
Timolol
1. Topical beta-blocker; reduces aqueous production. Apply BID.
2. Not a very potent IOP-lowering agent
3. Usually reserved for when IOP is close to OK, and you only need a few more mmHg.
The above agents can be (and often are) used together

# Maintenace surgical therapy

Many dogs will either not respond to medical therapy or will initially respond and then become refractory to medical therapy.
If surgery is going to be needed it is most effective if employed before significant optic nerve damage has been done.
Cyclodestructive procedures - reduce aqueous production; cyclocryosurgery (i.e., freezing) or cyclophotocoagulation (i.e., laser)
Drainage procedures. The primary procedure in this category is the gonioimplant. These procedures facilitate aqueous outflow. Primary problem is postoperative fibrosis of surgically created outflow path. The advent of perioperative antifibrotic drugs has reduced the incidence of this complication.
The prognosis for long term maintenance of vision is always bleak. However, the newer drainage procedures in conjunction with antifibrosis medication has resulted in maintenance of vision for several years in some cases.

# Neuroprotective therapy

All of the therapies just listed are aimed at reducing intraocular pressure. But as you’ll recall from the beginning of this topic, the optic nerve can continue to degenerate even if IOP is brought under control. Thus, the chief focus of modern glaucoma research is optic nerve protection. We currently have no “gold standard” for accomplishing this, but many things are on the drawing board that may well become clinical realities during your practice lifetimes, including:

NMDA antagonists
Tetrahydrocannabinol
Calcium channel blockers
Gingko biloba

# Salvage procedures

If goal is simply to make animal comfortable following irrevocable vision loss due to glaucoma:

Enucleation; few complications, assures no further eye problems
Evisceration with silicone prosthesis; few complications, but dog does retain cornea, conjunctiva, third eyelid, and lid margins, and can therefore still experience future problems with those structures (e.g. KCS, lid tumor, conjunctivitis, etc.) Strictly contraindicated in glaucoma secondary to infection or neoplasia
Intravitreal gentamicin injection; destroys ciliary body; often results in phthisis bulbi; a small percentage of dogs become chronically painful, necessitating enucleation. May be a good alternative when financial constraints are tight or animal is anesthetic risk. Strictly contraindicated in glaucoma secondary to infection or neoplasia.
Cyclocryosurgery - quick, easy inexpensive, but IOP may re-elevate
Chronic medical therapy (i.e., latanoprost, CoSopt, etc) - when owner is adamantly against surgery.

# Prognosis for opposite eye

Poor if glaucoma is primary. Usually presents unilaterally with second eye becoming affected within 8 months. Should consider prophylactic therapy of unaffected eye when patient presents for treatment of first eye, as the time to onset in the second eye is (on average) nearly 3 years when treated with timolol as a “preventative.”

← Cornea Anterior Uvea →