Glaucoma

• Cause: glaucoma represents a group of heterogenous diseases which, in dogs, are characterized by pathologically elevated intraocular pressure resulting in retinal ganglion cell death.
• Signs: ocular pain, blindness, episcleral congestion, conjunctival hyperemia, corneal edema, mydriasis.
• Diagnosis: ophthalmic examination including gonioscopy and tonometry.
• Treatment: ocular hypertensive medications and surgical options.
• Prognosis: guarded.
  Print off the owner factsheet on Glaucoma Glaucoma to give to your client.

• Usually present as a unilateral problem but, depending on cause, may be bilateral.
• Ocular pain.
• Redness around eye.
• Clouding of eye.
• Dilated pupil.
• Visual deficits (might not be obvious to owner if contralateral eye retains vision).

• Usually present as a unilateral problem but, depending on cause, may be bilateral.
• Ocular pain.
• Redness around eye.
• Clouding of eye.
• Dilated pupil.
• Globe enlargement.
• Visual deficits (might not be obvious to owner if contraleral eye retains vision).

• Depends on cause.

• Primary (inherited) glaucoma prevalent in several breeds.
• See Glaucoma: primary closed angle Glaucoma: primary closed angle and Glaucoma: primary open angle Glaucoma: primary open angle.

• Antiglaucoma medications can be costly.
• Surgical treatments are expensive.

• General anesthesia (if required for surgical treatment) Anesthesia: in ophthalmic surgery.

• Primary glaucoma.
• Uveitis Uveitis.
• Lens luxation Lens: luxation.
• Intraocular neoplasm Eye: intraocular neoplasia.
• Intraocular hemorrhage.
• Ocular melanosis Eye: uveal melanoma.

General

• Breeds predisposed to primary closed angle and lens angle glaucoma.
• Breeds predisposed to primary lens luxation.

Specific

• Presence of goniodysgenesis.
• Homozygosity for known mutations for primary open angle glaucoma and primary lens luxation.
• Uveitis.
• Cataracts Cataract.
• Previous intraocular surgery.
• Intraocular hemorrhage.
• Ocular melanosis.

• See also Glaucoma: secondary to anterior uveitis Glaucoma: secondary to anterior uveitis , Glaucoma: due to lens luxation Glaucoma: due to lens luxation , Glaucoma: primary closed angle Glaucoma: primary closed angle and Glaucoma: primary open angle Glaucoma: primary open angle.
• Normal intraocular pressure is a balance between aqueous humor production and outflow:
  • Aqueous humor is produced by the ciliary body processes by active secretion (mainly) and ultrafiltration.
  • Aqueous humor then traverses the posterior chamber via the pupil into the anterior chamber.
  • From the anterior chamber, the majority of aqueous drains via the iridocorneal angle.
  • The main components of this angle are the pectinate ligament and ciliary cleft which contains the sieve-like trabecular meshwork.
  • The majority of aqueous (//www.vetlexicon.com85%) filters through these structures and enters the angular aqueous plexus before entering the scleral venous plexus ('conventional' outflow).
  • A minority of aqueous (//www.vetlexicon.com15%) bypasses the aqueous plexus and reaches the scleral venous plexus via the choroid and suprachoroidal space.
  • Normal intraocular pressure in the dog is 10-25 mm Hg.
• In dogs, the only consistent risk factor for glaucoma amongst the group of heterogenous diseases is pathologically elevated intraocular pressure.
• Overproduction of aqueous humor is not a recognized phenomenon in dogs and, thus, all known forms of glaucoma relate to obstruction to aqueous humor outflow.
• Aqueous humor obstruction can occur at any point from its release into the posterior chamber to its ultimate drainage into the angular aqueous plexus and include the following:
  • Pupil block:
    • Iris bombe. Peripheral synechiae (adhesions between posterior iris and anterior lens capsule) for 360° in chronic uveitis.
    • Lens luxation and subluxation.
    • Vitreous prolapse (following lens removal or lens luxation).
  • Obstruction of entrance to iridocorneal angle:
    • Severe goniodysgenesis (pectinate ligament dysplasia) in primary closed angle glaucoma.
    • Obstruction by red blood cells (trauma), white blood cells and inflammatory debris (acute and chronic uveitis).
    • Anterior synechiae (chronic uveitis).
  • Obstruction within ciliary cleft:
    • Severe goniodysgenesis in primary closed angle glaucoma.
    • Undefined anatomical and biochemical changes in primary open angle glaucoma.
    • Collapse of ciliary cleft in all forms of glaucoma.
    • Neoplastic extension.
    • Obstruction by red blood cells (trauma), white blood cells and inflammatory debris (acute and chronic uveitis).
• Elevation of intraocular pressure causes interruption of vacular supply to optic nerve head and axoplasmic flow within optic nerve axons.
• Increase in glutamate levels may cause excitotoxicity-mediated retinal ganglion cell death.

• Variable dependent on cause.
• Acute in primary closed angle glaucoma and primary lens luxation.
• Chronic in anterior uveitis, neoplasia and ocular melanosis .

• Ocular pain.
• Blindness.
• Red/cloudy eye.

• Ocular pain.
• Blindness.
• Red/cloudy eye.

• Pain:
  • More obvious in acute glaucoma when IOP>50 mm Hg.
  • Abnormal vocalization, depression, head shyness, inappetence.
• Corneal edema   :
  • Mainly due to damage to corneal endothelial cells.
• Cornea vascularization  :
  • A deep 'brush border' presence of blood vessels may appear after a few days of acute glaucoma.
  • Superficial vascularization more common in cases of chronic glaucoma.
• Corneal striae  :
  • Due to breals in Descemet's membrane .
• Mydriasis  :
  • Results from paresis/paralysis of iris sphincter muscle.
    Pupil may be normal size or even miotic in uveitis glaucoma.
• Episcleral congestion  :
  • Common but not always present.
• Vision loss:
  • As a result of damage to retinal ganglion cells.
• Globe enlargement  :
  • As a result of chronic elevation of intraocular pressure leading to globe stretching.
  • Often a feature of congenital and primary open angle glaucoma.
• Intraocular hemorrhage  :
  • May result from glaucoma or lead to elevated intraocular pressure by obstructing aqueous humor outflow.
• Optic disk cupping  :
  • High intraocular pressure causes recession of optic nerve head towards lamina cribrosa.
• Retinal and optic nerve head atrophy.
• Phthisis bulbi:
  • Destruction of ciliary processes in chronic glaucoma may result in ultimate shrinking of the globe as aqueous humor production ceases.

• Ophthalmic examination Eye: examination for signs of above.

• Dependent on cause.

• Corneal endothelial disease (also causes corneal edema).
• Uveitis (also causes episcleral congestion).
• Pharmacological pupil dilation.
• Other causes of blindness Blindness (cataract, retinal disease, CNS disease).

• Emergency treatment. Primary closed angle glaucoma requires emergency treatment to lower IOP quickly. Options include:
  • Intravenous administration of hyperosmotic agents (eg 10% mannitol) which reduces intraocular pressure via an osmotic effect on the vitreous and aqueous.
  • Topical application of prostaglandin analogues (eg latanoprost Latanoprost , travoprost). Side effects include profound miosis and disruption of the blood-aqueous barrier. For these respective reasons, these drugs should not be used in cases of anterior lens luxation and anterior uveitis.
  • If these emergency measures fail to reduce intraocular pressure to within normal limits then aqueocentesis Paracentesis: aqueous (under sedation) will need to be considered.

• Numerous treatment strategies have been employed to treat canine glaucoma with varying degrees of success.

Medical management

Ocular antihypertensive medications

• Prostaglanding analogues (eg latanoprost 0.005%, travoprost 0.004%). Topical prostaglandin analogues are also used for longer-term treatment of glaucoma. They increase aqueous outflow and are commonly used 1-3 times daily. Side effects include miosis, break-down of blood-aqueous barrier and conjunctival hyperemia. They are contraindicated in cases of anterior lens luxation.
• Carbonic anhydrase inhibitors (eg dorzolamide Dorzolamide 2% and brinzolamide 1%). Used topically, these agents reduce aqueous humor production by inhibiting carbonic anhydrase within the ciliary epithelium. They are usually used 2-3 times daily.
• Beta-blockers (eg timolol Timolol 0.5%). These drugs also increase aqueous outflow and are usually used 2-3 times daily. Side effects include miosis, bradycardia and hypotension.
• Combination ocular hypotensive products are available which may enhance owner compliance when several drugs are recommended.
• Analgesia:
  • NSAIDs Analgesia: NSAID.
  • Opioids Analgesia: opioid.
• Prophylactic treatment:
  • Prophylactic treatment of the fellow eye has been shown to delay onset of primary glaucoma although it is not clear what the best treatment might be. Most ophthalmologists advise topical carbonic anhydrase inhibitors or beta-blockers (or both). Topical prostaglandin analogues are also sometimes used but might not be the best choice as they cause shallowing of the anterior chamber and narrowing of the iridocorneal angle.
• Antiinflammatory medications:
  • Indicated when intraocular inflammation is a component.
  • Topical and systemic NSAIDs and corticosteroids may be used.
  • See Glaucoma: secondary to anterior uveitis Glaucoma: secondary to anterior uveitis.

Surgical therapy

• For eyes that remain visual or have the potential for vision then surgical treatment can be considered when topical treatment alone is not sufficient to maintain IOP within acceptable limits. In cases of lens luxation then surgical lens removal is indicated (see Glaucoma: secondary to lens luxation Glaucoma: due to lens luxation ).
• The main aim of surgery is to maintain or restore vision and but, if successful, surgery may also eventually allow the frequency of necessary topical medications to be reduced.
• Surgical treatments work by either reducing aqueous humor production or increasing its drainage from the eye.
• Even following successful surgical treatment, relatively frequent topical medications are still usually required.
• Cycloablation.
• Gonioimplantation.
• Enucleation Eye: enucleation and evisceration.
• See Glaucoma: primary closed angle Glaucoma: primary closed angle for more information.

• Monitoring of both eye affected and contralateral at risk eye is required.
• Stable patients are usually examined at least every 3 months.
• If there is a change in treatment then re-examination is performed after one week to ensure satisfactory response to treatment.

Treatment

• Additional antiglaucoma medications and/or surgery may be required.

Monitoring

• If treatment failure then enucleation/evisceration is required for blind and painful eyes.

• Guarded prognosis but will depend on cause.
• Many affected dogs will require enucleation.

• Guarded.

• Irreversible collapse of ciliary cleft.
• Irreversible retinal and optic nerve degeneration.
• Poor response to human antiglaucoma medications.
• Inability to cycloablate entire 360° of ciliary processes.
• Occlusion of gonioimplants with fibrin, fibrosis of filtration 'bleb'.

Refereed papers

• Recent references from PubMed and VetMedResource.

Other sources of information

• BSAVA Manual of Ophthalmology.(2014) Gould D & McLellan G (eds). 3rd edn, pp 273-296.
• Veterinary Ophthalmology.(2013) Gelatt K, Gilger B, Kern T (eds). 5th edn, pp 1050-1145.
• For information on Genetic Testing Providers (labs) genetic tests, and tests by breed, visit International Partnership for Dogs (https://dogwellnet.com/).
• For a list of DNA tests available for certain breeds worldwide, visit Kennel Club Worldwide DNA tests: https://www.thekennelclub.org.uk/health/for-breeders/dna-testing-simple-inherited-disorders/worldwide-dna-tests/.