Canine Corneal Disease Study Guide

Overview and Clinical Importance

Corneal disease represents one of the most commonly encountered ophthalmic conditions in canine practice and is a high-yield topic for the NAVLE. The cornea is the transparent, anterior-most structure of the eye, essential for light refraction and vision. Because it is avascular and continuously exposed to the environment, the cornea is particularly vulnerable to trauma, infection, and immune-mediated inflammation.

Understanding corneal anatomy, pathophysiology, and the clinical approach to corneal disease is critical for both examination success and clinical practice. Corneal conditions range from simple superficial ulcers that heal within days to complex melting ulcers and descemetoceles requiring emergency intervention.

Corneal Anatomy and Physiology

The canine cornea averages 0.62 mm in thickness (approximately half the thickness of a dime) and consists of four distinct layers, each with unique properties affecting disease presentation and treatment.

Corneal Layer Characteristics

Ulcerative Keratitis (Corneal Ulcers)

Corneal ulcers are one of the most common ophthalmic emergencies in dogs. They are characterized by loss of corneal epithelium with exposure of underlying stroma. Classification is based on depth, duration, and underlying cause.

Etiology

Exogenous causes: Trauma (scratches, foreign bodies, cat scratches), chemical burns (shampoo, irritants), thermal injury

Endogenous causes: Keratoconjunctivitis sicca (KCS/dry eye), eyelid abnormalities (entropion, ectropion, distichiasis, ectopic cilia), lagophthalmos, trichiasis, epithelial basement membrane dystrophy

Classification by Depth

Clinical Signs

• Blepharospasm (squinting) - often the first sign noticed by owners
• Epiphora (excessive tearing) - if tear production is normal
• Conjunctival hyperemia (red eye)
• Corneal edema (blue-gray haziness)
• Corneal vascularization (indicates chronicity)
• Miosis (reflex uveitis from axonal reflex)
• Mucopurulent discharge (suggests infection or KCS)

Diagnostic Approach

1. Schirmer Tear Test (STT): Perform FIRST (before any drops). Normal is 15 mm/min or greater. Less than 15 mm/min indicates KCS. Note: Ulcerated eyes should have INCREASED tear production; low values in ulcerated eyes suggest KCS as the underlying cause.

2. Fluorescein Staining: Water-soluble dye adheres to hydrophilic stroma. Apply, blink to distribute, then rinse. Examine under cobalt blue light. Uptake confirms epithelial defect.

3. Complete Ophthalmic Examination: Eyelid evaluation for entropion/ectropion, distichia, ectopic cilia; third eyelid examination for foreign bodies; pupillary light reflexes; intraocular pressure (rule out glaucoma/uveitis).

4. Cytology and Culture: Indicated for deep, melting, or infected ulcers. Perform BEFORE fluorescein. Gram-positive cocci (Staphylococcus, Streptococcus) and Gram-negative rods (Pseudomonas) are most common isolates.

Treatment Protocols

Spontaneous Chronic Corneal Epithelial Defects (SCCEDs)

Also known as indolent ulcers, Boxer ulcers, or recurrent erosions, SCCEDs are chronic, non-healing, superficial corneal ulcers characterized by failure of epithelial adhesion to the underlying stroma.

Pathophysiology

SCCEDs result from a defect in the epithelial basement membrane and an abnormal hyaline acellular zone in the superficial stroma that prevents normal epithelial adhesion. The epithelium migrates over the defect but cannot anchor properly, creating characteristic loose, non-adherent epithelial edges.

Signalment and Predisposition

• Age: Middle-aged to older dogs (average 8-9 years)
• Breeds: Boxers are classically predisposed (hence 'Boxer ulcer'), but can occur in any breed
• Key feature: Superficial ulcer present for greater than 2 weeks despite appropriate therapy

Clinical Features

• Non-healing superficial ulcer (epithelium only)
• Loose, non-adherent epithelial edges - can be peeled back with cotton-tipped applicator
• 'Halo' or 'ring' pattern on fluorescein staining - dye extends under loose epithelium
• Variable pain (mild to severe blepharospasm)
• Variable corneal vascularization (may be absent or extensive granulation tissue)

Treatment

1. Debridement: Remove all loose, non-adherent epithelium using dry cotton-tipped applicators under topical anesthesia. The ulcer will appear larger after debridement - this is expected.

2. Grid/Punctate Keratotomy OR Diamond Burr Debridement: Creates microtrauma to superficial stroma, breaking up the hyaline zone and promoting epithelial adhesion. Success rate approximately 75-80% after first procedure. May require repeat in 2-3 weeks if not healed.

3. Post-procedure care: Topical antibiotics TID-QID, E-collar mandatory (critical - rubbing will dislodge healing epithelium), oral analgesics, recheck in 7-14 days

Keratoconjunctivitis Sicca (KCS/Dry Eye)

Keratoconjunctivitis sicca (KCS) is a chronic inflammatory disease of the cornea and conjunctiva resulting from inadequate tear production. It is one of the most common causes of corneal disease in dogs and is frequently under-diagnosed.

Etiology

Immune-mediated (most common): Lymphocytic-plasmacytic infiltration and destruction of lacrimal gland tissue

Drug-induced: Sulfonamides (trimethoprim-sulfa), etodolac, atropine

Neurogenic: Loss of parasympathetic innervation to lacrimal glands (CN VII lesions, otitis media)

Iatrogenic: Removal of third eyelid gland (cherry eye surgery - avoid gland excision)

Infectious: Canine distemper virus

Breed Predispositions

Cavalier King Charles Spaniel, American Cocker Spaniel, English Bulldog, West Highland White Terrier, Shih Tzu, Lhasa Apso, Pug, Boston Terrier, Miniature Schnauzer, Yorkshire Terrier

Clinical Signs

• Mucopurulent ocular discharge - thick, ropy, yellow-green (loss of aqueous component leaves mucus and lipid)
• Conjunctival hyperemia and chemosis
• Corneal changes: vascularization, pigmentation, scarring, ulceration
• Dull, lusterless corneal surface
• Blepharospasm (chronic irritation)
• Recurrent corneal ulcers

Diagnosis

Schirmer Tear Test I (STT-I): Gold standard. Measures basal and reflex tear production. Strip placed in lower conjunctival fornix for 1 minute.

Treatment

1. Lacrimostimulants (Cornerstone of therapy):

Cyclosporine A (Optimmune 0.2%): Immunomodulator that reduces lacrimal gland inflammation and stimulates tear production. BID application. May take 4-8 weeks for full effect. 80% of dogs respond.

Tacrolimus (0.02-0.03%): 10-100x more potent than cyclosporine. Used for cyclosporine non-responders.

2. Artificial tears/Lacrimomimetics: Supplement tear film; use preservative-free for frequent application

3. Topical antibiotics: If secondary bacterial infection or concurrent ulceration

4. Mucolytics (N-acetylcysteine): If excessive mucoid discharge

5. Pilocarpine (Neurogenic KCS): Oral cholinergic; stimulates lacrimal gland secretion

6. Parotid duct transposition: Surgical option for refractory cases; redirects salivary duct to eye

Chronic Superficial Keratitis (Pannus)

Chronic superficial keratitis (CSK), also known as pannus or Überreiter's syndrome, is an immune-mediated, progressive, bilateral corneal disease characterized by vascularization and pigmentation.

Pathophysiology

CSK is a cell-mediated (Type IV) immune response targeting corneal antigens. CD4+ lymphocytes are the predominant infiltrating cells. UV radiation is a major environmental trigger that modifies corneal antigens and activates the inflammatory cascade.

Breed and Environmental Predispositions

• Breeds: German Shepherd Dog (classic), Belgian Shepherd breeds (Malinois, Tervuren), Greyhounds, Border Collies, Siberian Huskies, Australian Shepherds
• Age: Typically 1-6 years at onset; younger onset = more aggressive disease
• Environment: High altitude and increased UV exposure significantly worsen disease (Colorado, Utah = high prevalence)

Clinical Features

• Bilateral, usually asymmetric
• Begins at temporal (lateral) or ventrolateral limbus
• Pink, elevated, vascularized granulation tissue advancing centrally
• Progressive corneal pigmentation (melanosis)
• NON-PAINFUL (unlike ulcerative keratitis)
• May have concurrent plasmoma (plasmacytic infiltration of third eyelid)

Treatment

1. Topical immunosuppressives (Mainstay): Cyclosporine (0.2-2%) or tacrolimus (0.02-0.03%) BID-TID; corticosteroids (dexamethasone, prednisolone) - use with caution, monitor for ulceration

2. UV protection: Dog goggles (Doggles) or limiting outdoor time during peak UV hours

3. Subconjunctival steroid injections: For refractory cases (triamcinolone, betamethasone)

4. Beta-irradiation or superficial keratectomy: Severe cases with significant pigmentation affecting vision

Corneal Dystrophies

Corneal dystrophies are primary, inherited, bilateral, non-inflammatory corneal opacities not associated with systemic disease. They are classified by the corneal layer affected.

Pigmentary Keratitis

Pigmentary keratitis refers to the deposition of melanin pigment on the corneal surface, most commonly seen in brachycephalic breeds. It results from chronic corneal irritation and inflammation.

Etiology

Pigmentary keratitis is a non-specific response to chronic corneal irritation. Contributing factors include:

• Medial entropion with trichiasis (nasal fold irritation)
• Lagophthalmos (incomplete blink/exposure)
• Keratoconjunctivitis sicca
• Exophthalmos/macropalpebral fissure
• Chronic irritation from any source

Breed Predisposition

Pugs are most severely affected (prevalence greater than 90% in some studies). Other brachycephalic breeds include Shih Tzu, Pekingese, Boston Terrier, English Bulldog, French Bulldog, and Lhasa Apso.

Clinical Features

• Brown-black pigment deposition on cornea
• Typically begins medially (nasal) and progresses centrally
• Often associated with corneal vascularization
• NOT painful unless concurrent ulceration
• Can progress to visual impairment if central cornea involved

Treatment

1. Address underlying cause: Treat KCS; correct entropion/medial canthoplasty; manage nasal fold trichiasis

2. Topical immunosuppressives: Cyclosporine or tacrolimus to slow pigment progression

3. Surgery: Medial canthoplasty (reduces palpebral fissure size), correction of entropion, nasal fold resection if contributing

4. Superficial keratectomy/cryotherapy: For severe cases with visual impairment; pigment may recur