8 Dermoids, also known as choristomas, are normal tissue in an abnormal location. They occur infrequently in puppies and are usually noticed at weaning or shortly thereafter because of the development of ocular irritation. Dermoids can be inherited in certain breeds such as the Dachshund, Dalmation, Doberman Pinscher, German Shepherd, and St. Bernard and are either unilateral or bilateral. Upon examination a mass of variable size and pigmentation with coarse hairs protruding from its surface is present at corneoscleral limbus and bulbar conjunctiva (Figure 8.1). Treatment is local excision; a superficial keratectomy is indicated if the dermoid extends onto the corneal surface. Incomplete excision usually results in regrowth. Normal size globes with smaller than normal corneas are rare. Microcornea is nearly always associated with microphthalmia and other ocular anomalies. Breeds affected include Australian Shepherd (merle ocular dysgenesis), Collie, Miniature and Toy Poodles, Great Dane, Old English Sheepdog, and St. Bernard (Figure 8.2). Affected individuals usually have a shortened palpebral fissure and a prominent nictitans which partially obscures the globe. Microcornea usually refers to a cornea that is <12 mm in horizontal diameter. Occasionally, central corneal mineralization and other ocular anomalies are present. Vision can be reduced or absent. There is no treatment available. Corneal opacities and persistent pupillary membranes (PPMs) are congenital corneal and iridal anomalies (Figure 8.3). The pupil is formed during the last one‐third of gestation and continues to develop for 4–8 weeks postnatally. If pupillary formation is incomplete or delayed, very fine white to pigmented remnants or strands of iris tissue originating from the iridal collarette or minor iridal arteriolar circle protrude off the surface of the iris and extend to other areas of the iris, the posterior cornea, the anterior lens capsule, or some combination thereof. If the cornea is involved, there will be deep round to oval endothelial opacities, sometimes containing pigmentation. Lens opacities involve only the anterior lens capsule and outer anterior cortex. Occasionally, corneal or lens opacities exist without the PPM attachment if the strand has previously atrophied. Generally, no treatment is necessary. Many breeds have been reported with PPMs; however, the Basenji is the only breed in which mode of inheritance has been established. Spontaneous chronic corneal epithelial defects, corneal erosion, recurrent erosion, persistent epithelial erosion, Boxer’s ulcer, indolent ulcer, refractory ulcer, or rodent ulcers are all synonyms to describe a clinical syndrome of recurrent superficial corneal ulcers that heal very slowly in the dog, and often recur. At least 24 breeds are predisposed to these ulcers. The corneal epithelium and its basement membrane appear abnormal, which accounts for the development of the erosion as well as its delayed healing (attachment) period. Most affected dogs are middle aged (5–7 years), and the Boxer breed accounts for a significant number of these ulcers (Figure 8.4). On examination the affected cornea demonstrates a superficial corneal ulcer with an overlying lip of non‐adherent loose corneal epithelium. Often, fluorescein or rose Bengal applied to these corneas will ooze or leak into stroma adjacent to the ulcer proper where the epithelium is not attached. Conjunctival hyperemia and a mild secondary iridocyclitis are often present. Treatment consists of removal of the loose epithelium under topical anesthesia with a dry cotton swab, followed by debridement of the exposed stroma to facilitate attachment. Diamond burr debridement is used often in preference to grid or multiple punctate keratotomy. Chemical debridement or superficial keratectomies are less commonly employed now. Recurrence in the ulcer in the same eye or the fellow eye is common given that these ulcers are caused by an abnormality of the epithelium and anterior stroma. Corneal ulcers are characterized by the loss of corneal epithelium and varying degrees of stromal loss, which determines the depth of the wound. Application of topical fluorescein to the bulbar conjunctiva and cornea results in the dye uptake by the ulcer (Figure 8.5). As fluorescein rapidly diffuses in the stroma and even the anterior chamber, observation of the stain should occur immediately after application. Topical fluorescein, adequate illumination, and some magnification are essential aids in the diagnosis and monitoring of corneal ulcers. Corneal ulcers follow trauma, shampooing, cat scratches, exposure (as with enlarged globe, impaired blink, or corneal sensitivity), keratoconjunctivitis sicca (KCS), and other causes. In the brachycephalic breeds, exophthalmia, lagophthalmia, incomplete blinks, and other factors contribute to corneal ulcerations (see Appendix B). Corneal ulcer may progress in size and depth (with or without therapy), and changes from a shallow to a deep stromal ulcer, descemetocele, and even to corneal perforation. Iris prolapse can occur within several hours. Corneal ulcers in the dog will often become infected by opportunistic or pathogenic bacteria, with Staphylococci and Streptococci species the most commonly isolated. Viral ulcers associated with canine herpesvirus (CHV‐1) have been documented in the dog, and fungal ulcers are uncommon (usually related either to a corneal foreign body or in an immunosuppressed patient). The main goals of medical therapy are: (i) to eliminate or prevent infection of the ulcer; (ii) to control or prevent the proteolytic and enzymatic digestion of corneal stroma; and (iii) to address the reflex uveitis that invariably accompanies the ulcer. Additionally, if the ulcer has perforated or is likely to because of its deep nature or the presence of keratomalacia, surgical stabilization can be warranted. The brachycephalic breeds are predisposed to central corneal ulcers that have the tendency to progress into the deeper stroma as well as recur (Figure 8.6). These ulcers must be under close clinical monitoring as they can rapidly deteriorate. Corneal exposure, lagophthalmia, reduced central corneal sensitivity, nasal fold trichiasis, distichiasis, inadequate blink rate, quantitative or qualitative tear deficiencies, and increased central corneal epithelial turnover contribute to the high prevalence of corneal ulcerations in brachycephalic breeds (see Appendix B). The history usually includes lacrimation, blepharospasm, eyelid swelling, conjunctival hyperemia, and a corneal opacity. Because brachycephalic patients have decreased central corneal sensation (compared with mesocephalic and dolichocephalic breeds), they often will not exhibit pronounced evidence of pain. An ophthalmic examination reveals a central or paracentral corneal ulcer that retains fluorescein. The corneal stroma can be grayish, irregular, and malacic (soft or friable). When the corneal stroma is completely lost within the ulcer, descemetocele occurs (characterized with fluorescein as a circle of dye staining the sides of the ulcer wall but not its bed). With rupture of the very thin descemetocele, iris prolapse follows. Therapy of the brachycephalic corneal ulcer includes topical antibiotics, autogenous serum, atropine (1%) or tropicamide (1%) for the secondary iridocyclitis, and systemic anti‐inflammatories and analgesics. Both topical antibiotics and serum are often instilled very frequently (sometimes hourly) for the first few days, to halt ulcer progression and promote healing. For those ulcers that progress (larger and/or deeper), immediate surgical intervention is recommended (usually a pedicle conjunctival graft). In contrast to the horse, dogs rarely develop fungal keratitis. The history is usually one of a corneal ulcer that persists in spite of intensive topical (and systemic) antibiotic therapy. There may be a history of trauma or a previous corneal foreign body. Affected dogs are often systemically or locally immunocompromised. Corneal ulceration is the most common clinical manifestation, but the occasional fungal corneal abscess occurs in dogs (Figure 8.7). Diagnosis is made based upon index of suspicion and the results of corneal cytology or biopsy (to demonstrate the presence of fungal elements) and culture. Therapy includes routine corneal ulcer therapy with the addition of topical antifungals, removal of the foreign and infected site, and, if necessary, a pedicle conjunctival graft. Prognosis is usually fair to good with appropriate therapy.
Canine Cornea and Sclera
Developmental and Congenital Defects
Dermoids
Microcornea
Persistent Pupillary Membranes
Corneal Ulcerations and Inflammation
Spontaneous Chronic Corneal Epithelial Defects
Corneal Ulcers
Corneal Ulcerations in Brachycephalic Breeds
Fungal Keratitis