Non-Ulcerative Diseases of the Cornea
World Small Animal Veterinary Association World Congress Proceedings, 2008
David A. Wilkie, DVM, MS, DACVO
The Ohio State University Veterinary Hospital Dept.
Columbus, OH, USA

All corneal lesions result in a decrease in the transparency of the cornea. There are only 4 basic changes that can result in a change in corneal transparency:

1.  Edema

2.  Pigmentation

3.  Scar

4.  Infiltrate

a.  Cellular

b.  Non-cellular or crystalline

Corneal Edema

Edema is of 2 types, focal and diffuse.

 Focal--is generally the result of a corneal ulcer. Diagnosis is by fluorescein dye.

 Diffuse--is generally due to endothelial damage. The cornea is fluorescein negative. The etiologies for diffuse corneal edema are:

 Anterior uveitis



 Breed related in the Chihuahua and Boston terrier (endothelial dystrophy)

 Anterior lens luxation

Intraocular pressure should be measured in all eyes with diffuse corneal edema.

Corneal Pigmentation

Pigmentation will result from any form of chronic superficial irritation. It is usually associated with corneal vascularization. Exceptions to this include:

Corneal Sequestration--Cat

Unique to cats. Seen more frequently in the brachycephalic (esp. Persians and Himalayans) cats. It occurs following chronic irritation or ulceration of the cornea and appears as a brown-black corneal lesion. If you see a black lesion on the cornea of a cat it is probably a sequestrum.

Painful, often vascularized, fluorescein negative. Has been associated with herpes keratitis. As the name suggests this is like any other sequestrum, it is a walled off area of dead tissue.


1.  Superficial keratectomy +/- supportive grafting techniques

2.  Topical antibiotics, atropine, and artificial tears following surgery

3.  Antiviral therapy


Intra- or extraocular (epibulbar (limbal) melanoma).

Corneal Scar

The diagnosis of a scar is made based on the history, presence of vascularization, and lack of pain.

Corneal Infiltrate

Cellular Infiltrates

These include:


Generally rare--varies with the species, but in general squamous cell carcinoma (horse, cow, cat) and lymphosarcoma (all species) are the most common.


Abnormalities such as a dermoid or epithelial inclusion cyst


Several specific diseases:

 Fibrous histiocytoma [Nodular Granulomatous Episclerokeratitis (NGE)]

 Non-neoplastic, inflammatory mass of the dog. Proliferative pink corneal mass usually at the temporal limbus in one or both eyes. Masses are subepithelial infiltrates of lymphocytes, plasma cells, and histiocytes. Most commonly seen in cocker spaniels, collies and collie crosses, pugs.


1.  Topical steroids--(dexamethasone 0.1% qid) initial treatment--not all are responsive

2.  Topical cyclosporine or tacrolimus

3.  Systemic azathioprine (Imuran ®) (2 mg/kg qd until remission then taper)--use if topical Dex does not control--need biweekly CBCs to monitor leukopenia

Chronic Superficial Keratitis (Pannus)

Previously called German shepherd or degenerative pannus. This is an immune-mediated disease that begins at the inferior temporal limbus. It results in corneal vascularization and pigmentation that will, if not controlled, advance across the entire cornea. German shepherds and their crosses are predisposed.


1.  There is no cure, only control

2.  Topical corticosteroids are the therapy of choice. Begin 4-6 x/day with topical 0.1% dexamethasone and taper to 1-2x/day as the disease is controlled. Therapy is life long.

3.  Topical cyclosporine or tacrolimus

4.  Decrease the dog's exposure to UV light as this seems to exacerbate the condition

Eosinophilic Keratitis

Unique to the cat and horse. Pink-red, raised lesion with a superficial white plaque that invades from the limbus and is non-painful. Uni- or bilateral. Diagnosis: cytology obtained by corneal scraping yields mast cells and/or eosinophils. This is pathognomonic.


1.  Topical corticosteroids: 0.1% dexamethasone 4-6x/day for 7 days then as needed to control the lesion. Therapy may be for life, but you should attempt to wean off the steroids at 2-3 months to see if the condition reoccurs.

2.  If corticosteroids do not control the lesion or it reoccurs while on corticosteroids, then megestrol acetate (Ovaban®) is the therapy of choice: 5 mg/cat SID for 4-7 days then rapidly taper the dose to a maintenance level of 1.25-2.5 mg/cat/week. (The side effects with Ovaban® include weight gain, mammary gland hyperplasia and neoplasia, diabetes mellitus, pyometra, and behavior changes.)

Non-cellular Corneal Infiltrates

These are infiltrates of crystalline material such as cholesterol or mineral. They often appear birefringent. They can be primary or secondary.


Corneal dystrophy. These are non-painful, non-vascularized, often bilateral, and occur in predisposed breeds. No treatment is required (See Table 1).


Corneal degeneration, the result of previous corneal inflammation (look for blood vessels) or associated with systemic diseases such as:


 Hypercholesterolemia of Cushing's


 Diabetes mellitus

 Chronic topical or systemic corticosteroids

Again no ocular treatment is required, but the systemic disease, if present, must be diagnosed and treated. The corneal lesion should regress with time if the initiating problem is corrected.

Table 1. Examples of corneal dystrophy in the dog.



Age of onset




4-12 months

Anterior stroma, central, lipid

Alaskan malamute

None or unknown

2 yrs and older

Para central, similar to beagle


None or unknown


Paracentral, stromal. Nebular, race track, white arc

Boston terrier


5-9 yrs

Corneal edema, endothelial dystrophy



6-13 yrs

Corneal edema, endothelial dystrophy

American cocker spaniel



Posterior polymorphous dystrophy



8-11 yrs

Corneal edema, endothelial dystrophy



1-4 yrs

Subepithelial lipid deposits



6 months-2 yrs

Gray round to oval (doughnut-shaped) opacity, stromal dystrophy

Shetland sheepdog


2-4 yrs

Multiple gray-white circular rings, superficial erosions

Siberian Husky

Recessive with variable expression


Gray round to oval (doughnut-shaped) opacity, stromal dystrophy

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

David A. Wilkie, DVM, MS, DACVO
The Ohio State University Veterinary Hospital
Dept.Vet Clin Sci
Columbus, Ohio, USA

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