Introduction

• Cause:
  • Edema
  • Pigment.
  • Calcium.
  • Lipid.
  • Scarring.
  • Cellular infiltrate.
  • Symblepharon.
• Signs: opacity of eye.
• Diagnosis: confirm opacity to be affecting cornea - identify underlying cause.
• Treatment: depends on nature of opacity.
• Prognosis: good to poor for resolution depending on nature and size of opacity.

Pathogenesis

Etiology

• May result from dysfunction of the corneal endothelium or epithelium, or changes in intraocular pressure, accumulation of fluid within the corneal stroma which is normally relatively dehydrated.
• Potential causes of endothelial dysfunction include iatrogenic resulting in compromise, endothelial dystrophy Cornea: endothelial dystrophy , uveitis and glaucoma Glaucoma (through alterations in intraocular pressure) and canine adenovirus 1 infection (also known as 'blue eye') Canine adenovirus type 1 disease .
• Breaches in corneal epithelium allow fluid from the precorneal tear film to gain access to the stroma.
• Edema - congenital: persistent pupillary membranes - variable size/distribution of affected areas +/- lens involvement Persistent pupillary membrane.
• Edema - acquired: iatrogenic endothelial compromise, endothelial dystrophy, uveitis Uveitis , glaucoma, lens luxation Lens: luxation , canine adenovirus 1 infection, secondary to erosion/ulceration.
• Cellular infiltrate: chronic superficial keratitis Chronic superficial keratitis.
• Pigment: pigmentary keratitis Pigmentary keratitis.
• Lipid deposition: corneal lipidosis Cornea: lipidosis , corneal lipid dystrophy.
• Symblepharon: adhesion between cornea and conjunctiva, or conjunctiva/conjunctiva, may obliterate fornix Symblepharon.
• Scarring Cornea: opacity.
• Calcium deposition associated with dystrophic calcification or secondary response to trauma.

• Damage to endothelial cells during intraocular surgery.

• Corneal endothelial cells are damaged by the associated intraocular inflammation.

• Glaucoma/uveitis.
• Changes in intraocular pressure affect fluid dynamics and result in over-hydration of the stroma.
• A proportion of infected dogs will develop endothelial damage.
• Antibody/antigen deposits form within the corneal endothelial cells.
• This does not occur with canine adenovirus 2 infection Canine adenovirus type 2 disease.

Predisposing factors

• Breeds at risk of glaucoma.

• Breeds at risk of lens luxation.

Specific

• Breed for endothelial dystrophy or blue eye with CAV-1 infection.

Pathophysiology

• Degeneration of corneal endothelial cells results in loss of endothelial cell pump function and subsequent bilateral corneal edema.
• Fluid accumulation underneath the corneal epithelium leads to the formation of bullae which rupture, resulting in corneal ulceration Ulcerative keratitis.

• Affected dogs intially develop an anterior uveitis which is of variable severity Uveitis.
• Antibody/antigen deposits form within the endothelial cells 10-14 days post-infection, resulting in a disruption of normal function.

Timecourse

• Most blue eye cases resolve in 30 days.
• Slow progression to total corneal edema in endothelial dystrophies (worsens with age).
• Endothelial cell pump damage, irrespective of cause, results in loss of corneal detergescence.

Diagnosis

Treatment

Prevention

Outcomes