Rhea V. Morgan, DVM, DACVO, DACVIM

Glaucoma is an elevation in intraocular pressure (IOP) that interferes with normal function of the eye. Normal intraocular pressure ranges from 11 - 20 mmHg in dogs and 11 - 24 mmHg in cats. IOP values vary depending upon the instrumentation used to measure them. IOP differences of > 8 mmHg between eyes should be considered significant.

High intraocular pressure damages the retina and optic nerve, which, in turn, causes loss of vision. In acute glaucoma of the dog, it is not unusual for IOPs to be > 50 mmHg and to range as high as 90 mmHg.

Glaucoma has both primary and secondary causes. Primary glaucoma is an inheritable dysfunction or deformation of the iridocorneal angle. Secondary glaucoma develops when an underlying ocular disease alters the normal outflow of aqueous.



  • Causes
    • Primary glaucoma occurs in many breeds of dogs and often arises spontaneously, usually in one eye first. The iridocorneal angle may appear structurally abnormal, as in goniodysgenesis or closed angle glaucoma. The iridocorneal angle may also appear physically normal, but its function is altered, as in open angle glaucoma.
      • Primary disorders are the most common cause of glaucoma in the dog, but are rare in the cat.
      • Rarely, congenital glaucoma may be found in puppies and kittens from developmental or induced abnormalities of the angle.
    • Secondary glaucoma arises with a variety of conditions
      • Anterior uveitis or panuveitis may predispose to glaucoma. Although IOP is often low with acute uveitis, it may become elevated with severe or chronic inflammation. Elevations in IOP develop with obstruction of aqueous movement (e.g. posterior synechiae) and with obstruction of the drainage angle with protein, cells, and inflammatory debris.
        • Chronic uveitis is the most common cause of glaucoma in the cat.
        • Glaucoma secondary to uveitis is also a common problem in the dog, and may accompany infectious diseases such as blastomycosis and borreliosis, or noninfectious diseases, such as pigmentary uveitis of golden retrievers.
        • Lens-induced uveitis also predisposes both the dog and cat to glaucoma.
      • Anterior lens luxations are often accompanied by acute, severe glaucoma. Forward displacement of the lens and vitreous creates a physical blockage to the movement of aqueous through the pupil, and may also interfere with normal drainage through the iridocorneal angle as the iris is displaced anteriorly.
        • Primary lens luxations are common in the terrier breeds, particularly the Jack Russell terrier, fox terrier, Tibetan terrier, miniature bull terrier, as well as the border collie.
        • Secondary lens luxations may either be a cause or be a result of glaucoma.
      • Hyphema from trauma, coagulopathies, and hypertension may also cause glaucoma.
      • Glaucoma may also arise with intraocular tumors.
      • Pigmentary glaucoma is a rather peculiar disease of older Cairn, West Highland white, and Scottish terriers, in which a benign progressive melanosis of the anterior uveal tract encroaches upon the drainage angle and decreases aqueous outflow.
      • Glaucoma can be both an early or late complication of intraocular surgical procedures, such as cataract extraction and lensectomy for luxated lenses.
  • Risk factors
    • Age - Glaucoma can develop in any age of animal. Primary lens luxations tend to occur in dogs between 3 and 7 years of age. Primary glaucoma usually affects middle-aged, adult dogs. Pigmentary glaucoma usually affects older dogs.
    • Breed/genetics - Over 30 different breeds of dogs are predisposed to primary glaucoma. They include the Alaskan malamute, American cocker spaniel, basset hound, beagle, Boston terrier, Bouvier de Flanders, chow chow, dalmation, English cocker spaniel, English springer spaniel, giant schnauzer, Great Dane, mastiff, miniature poodle, miniature schnauzer, miniature pinscher, Norwegian elkhound, Samoyed, shar-pei, shih tzu, Siberian husky, smooth haired fox terrier, Welsh springer spaniel, and wire haired fox terrier. Domestic short-haired cats and Siamese cats may also develop primary glaucoma.
      • Golden retrievers are predisposed to secondary glaucoma associated with pigmentary uveitis.
      • Cairn, West Highland white and Scottish terriers are predisposed to pigmentary glaucoma.
      • The Jack Russell, Sealyham, fox, miniature bull terrier, as well as the Tibetan terrier and border collie are predisposed to anterior lens luxations and secondary glaucoma.
    • Sex - Primaryglaucoma affects males and females equally. Middle-aged male cats are more prone to chronic iritis, which predisposes them to secondary glaucoma.
    • Geographic/environmental - No known risk
    • Other medical disorders - Ocular inflammation, infection, neoplasia, and hyphema can predispose the eye to glaucoma. Systemic disorders of coagulation that may produce hyphema or inflammation can also lead to glaucoma.
  • Prevention - Glaucoma is almost impossible to prevent in the initially affected eye. Primary glaucoma usually strikes without warning and can occur in eyes with either normal or abnormal appearing drainage angles. With primary glaucoma, prophylactic treatment of the second eye statistically delays the onset of glaucoma in that eye, but the future of the second eye is always uncertain.


  • Species affected - Glaucoma is more common in dogs than cats.
  • Presenting signs and historical problems
    • Glaucoma generally affects only one eye initially, and statistically the left develops primary glaucoma more often than the right. With primary glaucoma the other eye is usually at risk for developing glaucoma, but secondary glaucoma may be a unilateral disease.
    • The major complaint is a sudden change in the appearance of one eye. With unilateral disease, loss of vision may not be noted by the owner.
    • Blepharospasm, tearing, cloudiness to the cornea, and ocular redness are common clinical signs with acute glaucoma.
    • With chronic glaucoma buphthalmos may develop. Corneal edema and striations may be noted, the eye may be chronically red, the pupil is often dilated, and blindness may be more obvious.


  • General
    • Body condition - Normal
    • Vital signs - Usually normal, unless an underlying systemic illness is present.
    • Mucous membranes - Normal
    • Hydration status - Normal
  • Head and neck - No significant abnormalities
  • Eyes - A complete ocular examination is required to confirm the present of glaucoma. Cranial nerve reflexes, especially menace reflexes and papillary light responses (PLRs) are used to evaluate vision in the eye. Schirmer tear testing is performed, and the cornea is stained with fluorescein. If corneal edema allows it, both the anterior segment and posterior segment of the eye are evaluated.
    • Classic findings include episcleral injection, corneal edema, abnormalities in pupil size, slow or absent direct PLR and indirect PLR to the opposite eye, weak or absent menace response, epiphora and blepharospasm.

    • Aqueous flare may be noted with both primary and secondary glaucoma. Position of the lens may be altered. Pigmentary or inflammatory changes of the iris or the presence of a mass may be noted.
    • Examination of the optic nerve may reveal it is smaller in size than that of the opposite eye, and it may be dark and gray. The surface may be indented or cupped.
    • With chronic glaucoma, the globe may be enlarged, menace reflex and PLRs are absent, and episcleral injection and corneal edema often persist. Breaks in descemete's membrane (Haab's striae) may occur when the cornea has been stretched.

    • Evidence of retinal degeneration and optic nerve atrophy may be found.

  • Oral cavity - No significant abnormalities
  • Thorax (cardio-pulmonary) - No significant abnormalities, unless an underlying systemic disease is present.
  • Abdomen (gastrointestinal/urinary) - No significant abnormalities, unless an underlying systemic disease is present.
  • Reproductive system - No significant abnormalities
  • Lymph nodes - No significant abnormalities, unless an underlying systemic disease is present.
  • Integumentary system - No significant abnormalities
  • Neurologic examination - No significant abnormalities
  • Musculoskeletal examination - No significant abnormalities


  • Special examination techniques
    • Schirmer tear test and staining of the cornea with fluorescein are performed to rule out other causes of a red eye.
    • Tonometry is required to measure IOP, and to reach a definitive diagnosis of glaucoma. IOP cannot accurately be estimated with digital palpation. Two types of tonometry are available: indentation (Schiotz) and applanation (Tonopen, pneumatic tonometer). The Schiotz tonometer is the least expensive method, but requires a fairly large cornea, that the animal's head be positioned in an upward gaze position, and that the third eyelid not be prolapsed. Applanation tonometry is more expensive, but is also more accurate, can be performed on small corneas and with the head positioned in a normal position, and is technically easier to perform.
    • Gonioscopy involves the use of a special lens placed on the cornea so that the drainage angle can be viewed.

    • Gonioscopy is used to determine whether the iridocorneal angle is open, narrowed, closed or deformed.

    • It also helps identify pigmentation of the angle and encroachment of the angle by neoplasia. Gonioscopy may be difficult or impossible if the cornea is edematous. It should be performed on the normal eye in all dogs and cats suspected of having primary glaucoma. Although this test provides valuable information on the appearance of the drainage angle, it does not provide any information on how well the angle is functioning.
  • Clinical laboratory tests
    • CBC - No abnormalities, unless an underlying systemic disease is present.
    • Serum biochemical tests - No abnormalities, unless an underlying systemic disease is present.
    • Urinalysis - No abnormalities, unless an underlying systemic disease is present.
  • Diagnostic imaging
    • Ultrasound (other) - An ocular ultrasound should be considered if the cause of glaucoma cannot be confirmed and the posterior segment of the eye cannot be examined due to significant corneal edema, opacification of the anterior chamber or the presence of a cataract.


  • Differential diagnosis - Differential diagnoses include other causes of a red eye, corneal edema, enlargement of the globe and blindness.
    • Conjunctivitis and KCS
    • Corneal ulceration
    • Other causes of corneal edema
    • Uveitis
    • Scleritis
    • Exophthalmos
    • Lagopthalmos
    • Other causes of retinal degeneration or atrophy
    • Other optic nerve diseases
  • Recommended tests
    • Complete ophthalmologic exam
    • Tonometry
    • Gonioscopy
  • Summary of diagnostic criteria
    • Elevated intraocular pressure
    • Typical signs of acute glaucoma as listed under eye examination.
  • Prognosis
    • Prognosis for vision in the glaucomatous eye is guarded to grave. Prognosis for control of IOP long-term is also poor.
    • Prognosis for the second eye is variable, depending upon whether the disease is primary or secondary.



Because acute glaucoma can destroy vision in < 24 hours, rapid intervention is essential. The initial goal is to lower the IOP to < 50 mmHg as quickly as possible, and to lower eventually the IOP to < 30 mmHg.

Initial therapy of acute glaucoma involves the use of osmotic agents to shrink the vitreous and lower the IOP, the use of topical or oral carbonic anhydrase inhibitors to decrease the production of aqueous, the use of other topical anti-glaucoma agents to decrease aqueous production, and the use of topical corticosteroids to decrease inflammation.

Following immediate lowering of the IOP, the cause of the glaucoma must be addressed. Primary glaucoma usually requires interventive therapy, such as surgery, cryotherapy or laser ablation of the ciliary body. Treatment for underlying ocular or systemic disease is indicated in cases of secondary glaucoma.


  • Acute vs. chronic glaucoma - It is important to decide whether the glaucoma is acute or chronic. Acute glaucoma is considered an emergency and requires hospitalization or referral to an institution that can provide immediate therapy. Pressure elevations > 50 mmHg cannot be withstood for more than a few hours, or the optic nerve will be irreversibly damaged. Chronic glaucoma is not an emergency, and therapeutic options differ from those of acute glaucoma.
  • Medical options for acute glaucoma - Medical therapy is considered successful if IOP is lowered in visual eyes back down to normal (< 20 mmHg) and if IOP remains < 30 mmHg in blind eyes.
    • Administration of osmotic agents - Intravenous mannitol (1-2 g/kg IV over 30-60 minutes) or oral glycerine (1-2 g/kg PO) osmotically draw fluid from the vitreous and lower IOP within 45- 60 mins. They are most effective in primary glaucoma and are not often indicated in cases of secondary glaucoma.

      Effects of these drugs are transient. Both drugs may be repeated within 6 hs. If IOP does not decrease or if IOP rapidly rises again. Further repeated use is not helpful, and may induce a rebound increase in IOP if the animal is allowed to drink large amounts of water over a short period of time.
    • Administration of carbonic anhydrase inhibitors (CAH-I) - Both oral and systemic forms of CAH-Is are available. The oral forms are associated with more side effects. Preliminary research indicates that the two forms are not additive if used together.
      • Examples of oral forms include the following:
        • Dichlorphenamide 2-4 mg/kg PO BID-TID in the dog and 1 mg/kg PO BID in the cat; not readily available at present.
        • Methazolamide 2-4 mg/kg PO BID-TID in the dog and 1-2 mg/kg PO BID in the cat.
      • Examples of topical forms include the following:
        • Brinzolamide 1% BID-TID
        • Dorzolamide 2% BID-TID
      • Administration of prostaglandin analogues - These drugs lower IOP by increasing aqueous outflow through the uveoscleral pathway. They are contraindicated in the presence of anterior lens luxation or anterior uveitis because they cause dramatic miosis and increase any pre-existing uveitis. They are helpful to achieve rapid lowering of IOP, as a positive effect may be seen within 20 - 30 mins. An examples is latanaprost 0.005% SID-BID.
    • Administration of prostaglandin analogues - These drugs lower IOP by increasing aqueous outflow through the uveoscleral pathway. They are contraindicated in the presence of anterior lens luxation or anterior uveitis because they cause dramatic miosis and increase any pre-existing uveitis. They are helpful to achieve rapid lowering of IOP, as a positive effect may be seen within 20 - 30 mins. An examples is latanaprost 0.005% SID-BID.
    • Administration of other topical anti-glaucoma medications - Several classes of anti-glaucoma medications are available. They include the beta-blocking agents, the parasympathomimetics, the sympathomimetics, and the alpha-agonists.
      • The beta-blockers are commonly used in animals BID-TID. They have several advantages in that they are not irritating, do not alter the size of the pupil, do not exacerbate uveitis, and can be administered in both primary and secondary glaucoma. They are absorbed systemically, so must be used with caution, especially the nonselective beta-blockers, in animals with heart disease, asthma or other respiratory disorders.

        Nonselective beta-blockers include timolol, levobunolol, optipranolol, and carteolol. Betaxolol is a selective B1-blocker and is safer to use in cardiac or respiratory patients.

        Parasympathomimetic agents include the direct acting miotics (pilocarpine, carbochol) and the indirect acting miotics, such as demecarium bromide. These drugs are potentially effective, but are also irritating, worsen any existing uveitis, and are contraindicated in the presence of anterior uveitis, and are contraindicated in the presence of anterior lens luxations. Pilocarpine is available in concentrations of 1%, 2% and 4% and is administered q 1-8 hours. Demecarium bromide 0.125% is not available commercially, but may be obtained from compounding pharmacies. It is given BID.
      • Sympathomimetics (epinephrine, dipivefrin) are not very effective in animals and are rarely used.
      • Alpha agonists, such as apraclonidine, are also available. They are particularly helpful to treat acute spikes in IOP, such as acute glaucoma following intraocular surgery or laser procedures. They are rarely used as continuous therapy for glaucoma, because of their potential systemic side effects (e.g. blanching of the mucous membranes, decreased heart rate), When given in acute glaucoma, two drops of apraclonidine 0.5% are given two minutes apart. IOP may decrease within 30 mins.
    • Administrations of topical corticosteroids - If the cornea is not ulcerated, topical steroids are indicated to combat inflammation. Preferred medications include those of sufficient potency to control uveitis and with good penetration of the cornea. Prednisolone acetate 1% is administered q 4-8 hrs. Alternatively, dexamethasone 0.1% may be given q 4-8 hrs.
  • Surgical options for acute primary glaucoma - Surgeries are designed either to decrease the formation of aqueous or increase the outflow of aqueous humor.
    • Increasing the outflow of aqueous is accomplished by performing some sort of shunting procedure. Such procedures include insertion of a one-way valve that allows aqueous to exit into the episcleral space, iridencleisis where a segment of iris is repositioned under the bulbar conjunctiva, and the creation of a sclerotomy, which is creation of a hole from the anterior chamber to the episcleral layer that bypasses the drainage angle.
    • Procedures that are designed to decrease the amount of aqueous formed include laser or cryocycloablation of the ciliary body. With laser ablation, a diode or neodymium: yttrium: aluminum: garnet (ND:YAG) laser is used to deliver energy across the sclera that is absorbed by the pigment within the ciliary body. With cryotherapy, liquid nitrogen or nitrous oxide are applied to the sclera over the ciliary body, and the pigment of the ciliary body is preferentially frozen. Both procedures result in necrosis of the ciliary body.
    • These surgical procedures are most often applied to eyes that retain the possibility of vision. Although they can be performed in blind eyes, they have a significant incidence of side effects and may not permanently lower IOP. See surgical options for blind eyes below.
    • Anti-glaucoma medications are continued following these surgeries.
  • Treatment of acute secondary glaucoma
    • Treatment of secondary glaucoma involves instituting topical and/or systemic anti-glaucoma medications, topical corticosteroids, and also treating the underlying cause.
      • Anterior lens luxations are surgically removed
      • Appropriate therapy is started for anterior uveitis
      • Enucleation is often indicated for intraocular tumors
  • Treatment of chronic glaucoma
    • Medical therapy alone does not often provide permanent control of glaucoma. The most common exception is secondary glaucoma associated with anterior uveitis in cats.
    • Medical therapy of primary glaucoma must usually be followed by one of the surgical or ciliary ablative procedures described above (in potentially visual eyes) or by one of the more permanent surgical solutions (in blind eyes).
    • Surgical options for blind eyes with chronic glaucoma that are not controlled medically include the following:
      • Enucleation - The eye is removed and the eyelids are permanently sewn shut. An implant may be inserted in the orbit at the time of enucleation to provide greater cosmesis.
      • Aggressive laser ablation - Greater amounts of energy are applied to the ciliary body in an effort to cause more extensive necrosis and prevent recovery of the ciliary tissue. This procedure is usually reserved for unresponsive cases of primary glaucoma.
      • Evisceration and insertion of an intraocular prosthesis - The eye is surgically opened and all tissues other than cornea and sclera are removed. A black silicone ball is placed inside the fibrous tunic of the eye and the eye is sewn closed. All tissue removed from the eye is submitted for histopathology. This procedure is usually reserved for unresponsive cases of primary glaucoma in the dog, particularly when the owner does not allow an enucleation to be performed.
      • Intravitreal gentamicin injection - This procedure is performed only in dogs with unresponsive primary glaucoma, or dogs with quiet secondary glaucoma in which no active infection or tumor exists. It involves removal of 0.5 ml of liquefied vitreous and the injection of 0.4 ml of gentamicin (20 mg) with 0.1 ml (0.2 mg) dexamethasone sodium phosphate.


Most animals are sent home on topical and/or systemic anti-glaucoma medications and topical corticosteroids. The surgical options may be pursued immediately in eyes with the potential for vision, or may be considered days to weeks later in eyes that are permanently blind.

If therapy fails, vision loss is not life threatening, and most animal behave normally if only one eye is blind. The vast majority of animals also adjust very well to impaired vision or blindness, if both eyes are involved.



  • Following discharge from the hospital, an initial recheck is usually scheduled for 4-7 days later. IOP is measured, and the animal is evaluated for the possible return of vision. The degree of intraocular inflammation is also assessed. Medications are adjusted and new drugs may be added to the regimen if IOP is not controlled, or a surgical option may be chosen.
  • Over time IOP is measured on a continuous basis, at regular intervals, for example, q 2 wks, then q 4 wks, then q 8 wks, etc.
  • Surgical procedures performed in potentially visual eyes have a significant failure rate with time and may need to be repeated, or an alternative procedure may be considered.
  • If one eye is diagnosed with primary glaucoma, the second eye should be always be examined and started on prophylactic topical therapy. The drugs of choice for topical therapy include one of the CAH-Is or one of the beta-blockers. IOP is measured in the opposite eye at each recheck visit.


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