MAB RESOURCES · August 23rd, 2021

A Quick Guide to Identifying Types of Glaucoma in Patients

The following report documents different cases of glaucoma in varying species more frequently seen by hospitals within our community. The information outlined in this guide includes details about diagnostics, the different types of glaucoma, and varying causes.

Normal Aqueous Humor Dynamics

  • Aqueous Humor (AH) Formation – AH is formed by the ciliary body processes and it enters the posterior chamber, travels through the pupil, and exits the eye via the corneoscleral trabecular and uveoscleral outflow pathways. The continuous flow of AH supplies the avascular cornea with nutrients and removes waste products. In a normal eye, the AH production equals outflow, maintaining a normal pressure.

AH is an ultrafiltrate of plasma. The ciliary processes produce AH with a combination of active secretion, ultrafiltration, and simple diffusion. Active secretion, via the Na-K-ATPase pump, is the most important factor in AH production. This pump then drives the reaction: CO2 + H2O ↔ HCO3 + H+ which is catalyzed by carbonic anhydrase. Carbonic anhydrase is targeted in some glaucoma treatments (carbonic anhydrase inhibitors). When there is a breakdown in the normal blood-aqueous barrier, more proteins and prostaglandins are in AH, which manifests as flare. Therefore, flare is a diagnostic for uveitis.

The rate of AH formation is influenced by sympathetic and parasympathetic innervation to maintain steady-state IOP. An increase in intraocular pressure (IOP) will cause a decrease in production.

  • Aqueous Humor Outflow – AH movement out of the eye is dependent on both conventional and nonconventional outflow. Different species have varying dependence on each of the pathways, however dogs and cats rely more on conventional flow (dogs 85%, cats 97%). Conventional outflow is through the corneoscleral trabecular meshwork (TM), or via the iridocorneal angle, to the venous system. The “entrance” to the iridocorneal angle is through normal pectinate ligaments. Conventional outflow changes in response to IOP (as IOP increases, conventional outflow increases).

Outflow happens passively into the vessels or can occur actively with phagocytosis. Macrophages in the endothelium of the vessels can actively engulf larger particulate material. A malfunction of endothelial phagocytosis may be what leads to open-angle glaucoma.

Extracellular glycosaminoglycans (GAGs) are also important in the outflow. GAGs are normally there to help facilitate flow into the venous system. An increase or a change in these extracellular GAGs may cause resistance to normal flow and ultimately lead to an increase in IOP. These GAGs are also targeted in some glaucoma treatments.

Nonconventional outflow is through the uveoscleral outflow. The uvea acts as a sponge to absorb the AH and then exit the venous system. The rate of outflow can be affected by the “state” of the uvea: contraction of the ciliary body musculature can decrease unconventional outflow by decreasing extracellular spaces (this is why atropine can increase the IOP). Nonconventional outflow is independent of the IOP.

Glaucoma Diagnostics

  • Normal dog IOP: 15-20mmHg; higher IOP in the morning
  • Normal cat IOP: 19-23mmHg; highest between 9pm – 12am.
  • Normal horse IOP: 15-30mmHg
  • Normal rabbit IOP: 15-20mmHg; conflicting studies of when the IOP peaks.
  • Tonometry – Tonometry is the measurement of IOP. Direct tonometry (via an intraocular manometer) is very invasive, so all of our clinical techniques perform indirect tonometry which is an estimation of IOP via the measurement of corneal tension. In other words, the tonometers we use on a daily basis measure the cornea’s response to the pressure inside of the eye. Therefore, corneal disease & thickness can affect IOP readings. Other factors that can affect IOP readings include: pressure on the eyelids (and subsequently the eye), pressure on the neck/jugular vein, stress of the patient, sedation, head position (especially important in the horse), experience of the practitioner, and circadian rhythm
    • Applanation Tonometer (AT) – AT measures the force required to flatten (or applanate) a constant area of the cornea. Eyelids are gently retracted using a non-dominant hand (do not put pressure on the globe). The dominant hand holds the AT perpendicular to the cornea such that the footplate makes complete & parallel contact with the cornea without visibly indenting the cornea. Readings from the central 2/3 of the cornea are most accurate. If the coefficient of variance is greater than 5%, repeat the measurement. This tends to be very accurate in the physiologic range but tends to overestimate IOP in the low range and underestimate in the high range in dogs & cats.
    • Rebound Tonometer (RT) – With a RT, a small probe is rapidly and electromagnetically propelled, from a fixed distance away from the cornea (3-5mm), to contact the cornea before returning (rebounding) to the instrument. The instrument assesses how fast the probe returns and then measures the IOP based on this speed & deceleration. TonoVet has been calibrated for dogs, cats, and horses and it is important to select the appropriate setting. Advantages include: topical anesthesia is not necessary and the small probe is suitable for very small eyes. Additionally, RT may be more accurate than AT in cats. A disadvantage is that the probe must be held such that the probe is horizontal, which prevents use in recumbent patients.
  • Gonioscopy – Gonioscopy allows visualization of the entrance to the iridocorneal angle (ICA). It is not possible to visualize this directly in the dog because of the scleral shelf, so a goniolens is necessary to refract light appropriately. Gonioscopy can differentiate open from closed-angle glaucoma. Additionally, it can identify pectinate ligament dysplasia which may predispose a dog to develop glaucoma. However, it only allows visualization of the opening of the angle (and doesn’t inform of the entirety of the angle). There is controversy on how informative this diagnostic is. (Often the ICA can be visualized with a slit lamp in the cat and horse.)

Pathophysiology of Glaucoma

  • The hallmark finding in glaucoma is retinal ganglion cell (RGC) death. RGCs are the cells that ultimately coalesce to form the optic nerve. Therefore, glaucoma can be considered an optic neuropathy. There is a condition of normotensive glaucoma in people. People with this disease have progressive optic nerve damage despite pressures staying within the normal range. This has not been documented in our patients at this point, but that may partially be due to our inability to pick up these signs in our patients.
  • Charlie Martin defines glaucoma as “an elevation in IOP beyond that which is compatible with healthy ocular tissues. Since many conditions have the potential to increase IOP, glaucoma should be considered a sign, rather than a disease, per se.” (Martin 1983)
  • Primary closed/narrow-angle glaucoma (PCAG) – This is the most common type of canine glaucoma. Pectinate ligament dysplasia (PLD) is associated with the development of PCAG in many breeds. PLD is the lack of rarefaction of the pectinate band to form normal pectinate ligaments at the entrance to the ICA. In spite of this finding, the primary mechanism for elevated IOP is poorly understood in PCAG but may have something to do with the inherent anatomy of the patient’s eye, including anterior chamber depth, thicker lens, lens position, and overall axial length of the globe. Typically, PCAG leads to acute pressure spikes. IOP monitoring will unlikely identify these patients prior to a pressure spike. PCAG is always bilateral.
  • Primary open-angle glaucoma (POAG) – This is the most common type of glaucoma in people. POAG may lead to decreased outflow through the trabecular meshwork of the ICA due to extracellular matrix changes preventing normal outflow. Typically, POAG leads to a more gradual pressure increase. IOP monitoring may identify these patients earlier in the disease. Beagle POAG is used as a human research model and the gene mutation is identified. POAG is always bilateral.
  • Primary congenital glaucoma – This occurs in patients less than one year and is often accompanied by multiple anterior segment anomalies. Typically patients become very buphthalmic due to the abundance of elastin fibers in the young sclera. Congenital glaucoma may or may not be bilateral.
  • Secondary glaucoma – This is the most common cause of feline and equine glaucoma. Secondary glaucoma occurs when another disease process leads to increased IOP. The underlying disease process leads to obstruction to normal AH flow either through the pupil, through the pectinate ligaments (entry to the ICA), or through the trabecular meshwork with the ICA.

Dog Glaucoma

  • PCAG in dogs – Typically these patients present with acute pressure spikes. It is unknown what leads to the acute pressure spike. However, within days of the increased pressure, permanent changes are starting to occur that make the long-term prognosis for vision even poorer, including further angle closure and anterior synechia.
  • Breeds of highest prevalence in NA – ACS, Basset, Chow, Shar Pei, Boston, Wire Fox Terrier, Norwegian Elkhound, Husky, Cairn, Poodle, Samoyed, Bichon, Shih Tzu, Australian Cattle Dog
  • Treatment for acute congestive glaucoma – When a patient presents acutely with a pressure spike and there is a chance for vision, emergency treatment is indicated:
    • Topical therapy – Hourly topical therapy to bring pressures down quickly is often effective.
      • Prostaglandin analogues (PA)[ex: Latanoprost] – PA are converted to PGF2α in the eye. The mechanism for PGF2α causing a decrease in IOP is not well understood. PA are thought to increase the uveoscleral (unconventional) outflow, but there may be some evidence it also increases conventional outflow. Both of these mechanisms are likely related to the remodeling of the extracellular matrix by MMPs. Miosis and hyperemia are expected with PA; with very frequent dosing uveitis can occur. Glaucomatous eyes can see a 50% decrease in IOP.
      • Carbonic anhydrase inhibitors (CAI)[ex: Dorzolamide] – CAI block the aforementioned reaction in the ciliary body that produces AH. We do not recommend using systemic CAI as topicals have been shown to be just as effective and do not cause systemic side effects. Side effects can include topical irritation (burning) or keratitis.
    • Osmotic agents [ex: Mannitol] – Following IV administration, osmotic agents are distributed in plasma increasing the osmolarity of the extracellular fluids compared to the intraocular space and therefore pulls fluid primarily from the vitreous body to decrease the IOP and open the ICA. Osmotic agents also decrease AH production. Side effects involve quickly expanding the extracellular fluid volume especially in cardiac patients as well as decreased clearance in renal patients. Dose 1-2g/kg infused over 20-30min and can last 6-10 hours. Keep water away for 4 hours.
    • Paracentesis – Manually removing AH can decrease IOP quickly, however can also come with significant side effects including bacterial introduction, uveitis, hyphema, and retinal detachment.
  • Treatment for chronic glaucoma – Once the acute patient’s pressure is in the normal range or if the prognosis for vision is nil (buphthalmic, optic nerve damage) then chronic therapy is indicated. Typically latanoprost is used twice daily, dorzolamide 3 times daily, or Cosopt (dorzolamide + timolol) 2-3 times daily.  Be careful with Timolol in cardiac or asthmatic patients. Ineffective treatments in dogs include Timolol alone, epinephrine, or pilocarpine.
  • Treatment for the unaffected eye – In primary glaucoma, treating the unaffected eye twice daily has been shown to slow progression from 8 months to 32 months. The studies used a beta-blocker but dorzolamide is also commonly used.
  • Treatment for visual eyes not responsive to medications/having spikes – Once the eye is having IOP spikes on “max” medications, surgery can be considered. Surgery can have significant side effects so is appropriate in the right dog with the right owner.
    • Cyclophotocoagulation (CPC) – Laser CPC (via diode or Nd:YAG) destroys the ciliary body epithelium, thereby decreasing AH formation. This can be performed transclerally or via endoscopy.  In theory, endoscopic CPC should have less collateral damage and better results.
    • Gonioshunt – A shunt can be placed into the anterior chamber, draining fluid subconjunctivally. Shunts have been created that have a pressure-sensitive valve such that when the pressure rises (for example above 12mmHg) the valve within the shunt opens to drain fluid.
  • End-stage treatment – End-stage treatment is appropriate for dogs whose pressures are uncontrolled on medications and are also blind. This includes enucleation, gentamicin injection, or evisceration.
  • Secondary glaucoma in dogs – There are several causes of secondary glaucoma in dogs. Glaucoma occurs when something (for example a mass, luxated lens, or cells) physically obstructs normal outflow or when chronic inflammatory changes permanently change the intraocular structures. These changes can include changes to the extracellular matrix of the ICA or uveoscleral outflow, formation of posterior synechia, or formation of preiridal fibrovascular membranes. Treatment for secondary uveitis involves treating the underlying cause, if possible, as well as glaucoma treatment. However, some of our treatment options are limited.
    • Uveitis
    • Pigmentary Uveitis/Golden Retriever Uveitis
    • Ocular melanosis of Cairn Terriers
    • Intraocular mass
    • Anterior lens luxation
    • Aphakic/Pseudophakic

Cat Glaucoma

  • Primary glaucoma in cats – PCAG and POAG are very rare in cats. A few purebreds are reported to have primary glaucoma including the Siamese, Persian, European Shorthair, and Burmese.
  • Congenital glaucoma in cats – This is also rare in cats.
  • Secondary glaucoma in cats – This is the most common cause of glaucoma in cats.
    • Uveitis – This is the most common cause of secondary glaucoma in cats, with most of the cases due to chronic idiopathic lymphocytic-plasmacytic uveitis.
    • Diffuse iridal melanoma – This is the second most common cause of secondary glaucoma.
    • Anterior lens luxation (ALL) – Although ALL is fairly common in cats with chronic uveitis, this rarely leads to glaucoma in cats due to the size of the anterior chamber.
    • Aqueous misdirection/malignant glaucoma – This is a unique syndrome in cats that causes a constellation of anatomical changes in the eye, leading to increased IOP. AH becomes misdirected into the vitreous humor (rather than the anterior chamber). The increase in vitreal pressure causes anterior displacement of the lens and marked shallowing of the anterior chamber. Clinical signs include mydriasis and a shallow anterior chamber with an elevated IOP.
  • Glaucoma treatment in cats – If possible, treat the underlying condition. Dorzolamide and Dorzolamide/Timolol are effective in cats. Brinzolamide and latanoprost have been shown in some studies to not be effective. Other treatment options are limited in cats due to the risks of intraocular sarcoma including cyclophotocoagulation, gentamicin injection, and intrascleral prosthesis (evisceration).

Horse Glaucoma

  • Horse pathophysiology is different than small animals in that their uveoscleral outflow is a much higher percentage of AH drainage. Corneal edema tends to occur early in the process, while vision loss is often much later as compared to small animals. Additionally, horses often don’t act painful with glaucoma. Accurate pressure measurement can be made with an AT or RT, but auriculopalpebral blocks should be performed to minimize tension from the eyelids. The head should be held above the heart.
  • Secondary glaucoma in horses – This is by far the most common cause of glaucoma in horses. In most cases, the primary cause is Equine Recurrent Uveitis (ERU).
  • Glaucoma treatment in horses – Treatment involves treating the underlying cause as well as a glaucoma treatment. PA have not been shown to be helpful in horses, so we are limited to CAI. Laser and shunt treatment is also an option for visual eyes.

Rabbit Glaucoma

  • Hereditary glaucoma in the New Zealand white rabbit has been studied extensively and the gene has been identified. These rabbits have PLD. Rabbits often become buphthalmic and develop corneal edema. However, their pressures often return to normal with chronicity due to ciliary body degeneration. Rabbits rarely show pain with glaucoma.


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