Ординатура / Офтальмология / Английские материалы / Slatter's Fundemental of Vetrinary Ophthalmology 4th edition_Maggs, Miller, Ofri_2008

If the iris is incorporated into the healing wound, an anterior synechia is formed (Figure 10-23, B). If the iris is carried out of the wound, iris prolapse results (Figure 10-23, C).

Medical treatment for stromal ulcers and descemetoceles is similar to (although usually more intensive than) that for simple ulcers: An initiating cause should be sought and removed or controlled if possible, broad-spectrum topical antibiotic and mydriatic therapy should be initiated, and an Elizabethan collar should be provided. Stromal ulcers should be topically medicated with antibiotics as often as hourly for the first 1 to 2 days. If the ulcer is deeper than half corneal thickness, it will also benefit from surgery because the corneal stroma has only a limited ability to regenerate, and healing is slow, often requiring fibrovascular infiltration. This process may take weeks if it occurs spontaneously from the limbus but can be rapidly provided by conjunctival grafting.

Conjunctival grafts provide the following advantages:

•Mechanical support for a thin or weakened cornea

•A continuous supply of serum, which contains anticollagenases and growth factors

•An immediate source of actively replicating fibroblasts for collagen regeneration in the stroma

•A route for systemic antibiotics to be delivered to the corneal ulcer

Conjunctival grafts are somewhat tedious and time-consuming to perform and require advanced training, excellent magnification, correct instrumentation, access to and familiarity with use of 7/0 or smaller suture material with a swaged-on, spatulatipped needle, and knowledge of basic microsurgical principles. In most cases the patient needing a conjunctival graft should be referred to an ophthalmologist. Probably the most difficult skill to acquire is judgment of depth for placement of corneal sutures. Ideally, they should be placed approximately three-quarter corneal thickness and without penetrating the anterior chamber.

There are at least five broad types of conjunctival grafts:

•Island or free grafts (Figure 10-25, A and B)

•Complete or 360-degree grafts (Figure 10-25, C and D)

•Simple advancement or hood grafts (Figure 10-26, A)

•Rotational pedicle grafts (Figure 10-26, B)

•Bridge grafts (Figure 10-26, C)

Advancement-type (hood or 360-degree) grafts are probably easiest to harvest and place; however, rotational pedicle grafts more easily reach a defect in the central cornea. For rotational pedicle grafts, dissection is typically begun with tenotomy scissors at the temporal bulbar conjunctiva (Figure 10-27). A strip of conjunctiva of sufficient length and width to reach and cover the ulcer is freed from the underlying Tenon’s capsule. The conjunctival graft should be thin and mobile. A useful rule of thumb is that if tenotomy scissors can be readily visualized through the conjunctiva, the graft is thin enough. Corneal epithelium should be gently débrided for approximately 1 mm around the ulcer before suturing the graft to ensure union between the subconjunctival tissue of the graft and the corneal stroma in the ulcer bed. Débrided material may be submitted for cytologic and microbiologic examination. The graft is sutured to viable cornea surrounding the ulcer with simple interrupted sutures. An alternative approach is to tack the graft with four to six simple interrupted sutures and then oversew the graft perimeter with a

CORNEA AND SCLERA 187

A B

C D

FIGURE 10-25. A, A conjunctival island graft is harvested from the palpebral conjunctiva with use of a chalazion clamp for tissue fixation. B, The island graft is sutured into the corneal defect around its whole perimeter. C and D, A 360-degree conjunctival graft is harvested by complete perilimbal incision and centripetal advancement of conjunctiva. This graft type should be reserved for large corneal defects and is usually a globe salvage technique because scarring is commonly extensive. This graft does not require corneal sutures, although they can aid in reducing the chance of dehiscence.

A B

C

FIGURE 10-26. A, A conjunctival advancement graft is harvested from the bulbar conjunctiva adjacent to the corneal defect. This works best for paraxial corneal defects. B, A rotational pedicle graft in which a conjunctival pedicle is harvested from the lateral bulbar conjunctiva and rotated over the corneal defect. These grafts provide support and vascularity to axial defects. C, A conjunctival bridge graft is also harvested from bulbar conjunctiva but is left attached at both ends to enhance the vascular supply and equalize retraction forces that may cause dehiscence. In all three graft types, the conjunctiva is moved to cover the corneal defect in the direction of the arrow.

simple continuous pattern. Additional sutures at the limbus may help secure the graft. It is not essential to close the rent in the bulbar conjunctiva; however, doing so tends to reduce postoperative pain. The rent can be closed with a simple continuous pattern.

A B

C D

FIGURE 10-27. Fornix-based advancement flap for smaller lesions near the limbus. A, A small limbal incision is made adjacent to the lesion. B, The flap is undermined using blunt dissection. C, Parallel or slightly divergent conjunctival incisions are made toward the fornix, with the flap width sufficient to cover the corneal lesion. D, The conjunctival flap is advanced centrally to cover the corneal lesion and sutured in place with simple interrupted sutures of 7/0 to 9/0 polyglactin.

Medical therapy for ulcerative keratitis is continued, and the graft can be trimmed when the cornea is healed (Figure 10-28). Trimming is usually done at least 6 to 8 weeks after graft placement, although thin grafts may slowly integrate with the cornea and not require trimming. Use of topical corticosteroids to minimize scarring and reduce vascularization was traditionally recommended. More current information suggests that avascularity is the natural state for the cornea and will be regained spontaneously as the biologic need for blood vessels wanes. Cyclosporine (2% solution) does have some antiangiogenic properties and may be a safer alternative if anything is needed.

Other types of conjunctival grafts vary mostly in extent of dissection. Free or island grafts provide mechanical support to the cornea and may be sutured around their whole perimeter, thus ensuring a good “seal”; however, they lack the vascular advantages of other grafts. The 360-degree graft is unique in that it does not require corneal sutures; rather, the free con-

junctival edges are simply apposed to each other with horizontal mattress sutures of 6/0 or 7/0 polyglactin 910 (see Figure 10-25, C and D). Although this feature makes the graft technically easier to perform, early graft retraction is the major disadvantage. The 360-degree graft may be necessary, however, for very large central corneal ulcers.

TEMPORARY TARSORRHAPHY VERSUS THIRD EYELID FLAP. Third eyelid flaps have been used widely for treatment of ulcers. Although they do provide a “bandage” that reduces desiccation and frictional irritation of the cornea by the upper and lower eyelids, they are also associated with some unwanted and potentially deleterious effects. Penetration of medications through or around the third eyelid to the affected cornea is questionable at best; indeed the anterior face of the third eyelid provides a slick, and direct “chute” to the nasolacrimal puncta. Inability of the owner and clinician to monitor progress or, more important, worsening of the ulcer behind the third eyelid is another serious limitation of this technique. Some of the more serious, progressive ulcers presented to veterinary ophthalmologists have developed behind a third eyelid flap.

In comparison, a temporary lateral tarsorrhaphy is extremely easy to perform, provides adequate corneal protection, and allows medication and monitoring of the ulcer (Figure 10-29). A temporary tarsorrhaphy is performed using 3/0 or 4/0 silk or braided nylon on a 3⁄4- or 1⁄2-curved, cutting micropoint needle, with the aid of 3µ to 5µ magnification. The upper eyelid is grasped gently with fine tissue forceps, and the needle is passed

A B

through the skin, entering at the haired-nonhaired junction approximately 3 mm from the eyelid margin and emerging just anterior to the meibomian (tarsal) gland orifices, which appear as a gray line of small circles along the margin. Care is taken not to penetrate the conjunctiva, as doing so would cause suture to rub on the cornea. The suture is then continued through the lower lid, entering just anterior to the meibomian gland orifices and emerging at the haired-nonhaired junction. A mattress suture is completed by passing of the needle back through the lower and then upper lids in an identical manner approximately 5 to 7 mm medial to the point where the original “bites” were taken. The suture should be knotted firmly to further reduce the chance of corneal contact with the suture if “gapping” of the eyelids occurs. This completes a horizontal mattress-type pattern in which the knot is on the upper lid and less likely to be coated with ocular secretions. Usually one or two mattress sutures in this style beginning at the lateral canthus will close the lids to an extent that still permits monitoring and topical treatment medially but provides adequate corneal protection.

CYANOACRYLATE ADHESIVES (TISSUE GLUE). In some cases medical-grade ophthalmic cyanoacrylate adhesives may be used as an alternative to surgery. These provide structural support for deep stromal ulcers but none of the biologic advantages of conjunctival grafts. Cyanoacrylate has some inherent antimicrobial properties and helps stimulate vascular ingrowth but should be reserved for ulcers in which the health of the surrounding stroma is adequate and certainly not malacic. The technique is simple, but optimal position of the globe should be obtained to avoid inadvertently gluing adnexal structures. The patient is anesthetized and the eyelids are held open with a wire eyelid speculum. To facilitate adhesion, the corneal wound edges are gently débrided of epithelium, and the ulcer bed is cleaned and dried very gently with sterile cellulose sponges. A single drop of cyanoacrylate is applied through a 27or 30-gauge needle or painted onto the ulcer with a tuberculin syringe lacking a needle. The smallest drop can be generated by turning rather than pushing the plunger. The goal is not to fill the entire defect but rather to apply a thin coat over the ulcer bed and adjacent normal cornea for approximately 1 mm. The glue is typically extruded within 7 to 14 days as corneal blood vessels and/or epithelium migrate underneath it. A soft contact lens and/or a partial temporary tarsorrhaphy may be placed for added protection and to reduce frictional irritation from the rough glue surface.

PROTEASE INHIBITORS. Corneal “melting” (or malacia) is one of the most devastating consequences of severe ulceration as well as a prerequisite for stromal involvement. Collagenases are enzymes produced by certain bacteria, especially gramnegative organisms such as Pseudomonas spp. They are also elaborated by degranulating neutrophils and damaged corneal stromal or epithelial cells. Therefore deep (stromal) ulcers are assumed to be infected until proven otherwise. For patients with deep ulcers and for which surgery is not an option, protease inhibitors may be applied topically. Anticollagenase products are used in hope of inhibiting corneal melting. Acetylcysteine was once widely advocated for this purpose. More recently, autologous serum has been promoted as a preferred product. In addition to serum’s broad-spectrum anticollagenase properties, it also contains numerous growth factors assumed to be beneficial.

Serum is harvested from a venous blood sample collected aseptically and allowed to clot in a red-top tube. After centrifugation, serum is separated and stored in a sterile multidose

CORNEA AND SCLERA 189

vial or commercially available eyedrop container. Autologous serum can then be applied to the infected eye as needed (as frequently as every 30 to 60 minutes for a rapidly melting corneal ulcer). Serum should be stored in the refrigerator and replaced every few days.

Treatment of Indolent Corneal Ulcers in Dogs

Indolent ulcers (also known as refractory or “boxer” ulcers, spontaneous chronic corneal epithelial defects, and recurrent erosions) are a unique type of superficial ulcer in dogs that is frustrating for veterinarians and clients alike. This type of ulcer is due to a failed union between epithelial basement membrane and the anterior layers of the corneal stroma and, defined as such, has been proven to occur in dogs only thus far, although a clinically similar ulcer has been described in horses. These ulcers are typically chronic, superficial, noninfected, and minimally to moderately painful. They usually vascularize slowly if at all and are characterized by a nonadherent lip of corneal epithelium at the ulcer perimeter that is easily débrided with a cotton-tipped applicator (Figure 10-30). The epithelial lip often produces a characteristic “halo” fluorescein staining pattern because the stain runs under and is then seen through the lip (Figure 10-31). Indolent ulcers, which are seen regularly in

FIGURE 10-30. Indolent corneal ulcer in an elderly golden retriever. Note the indistinct ulcer margins and the mild corneal edema. There is also some superficial vascularization. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

FIGURE 10-31. The same indolent corneal ulcer as in Figure 10-30, here shown after fluorescein staining. Note the indistinct manner in which the ulcer bed stains and that there is a “halo” of stain rather than a stained area with sharp borders. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

older dogs of any breed and boxer dogs of any age, are believed to represent a defect in either the epithelial basement membrane or, more likely, the anterior stromal surface that prevents adhesion between these two structures. Diagnosis relies on characteristic signalment, chronicity, clinical appearance, and staining pattern of the ulcer as well as the ease with which the epithelium is débrided.

Grid keratotomy is the treatment of choice for indolent ulcers (Figure 10-32). Indolent ulcers should probably be pretreated for a few days with a broad-spectrum ophthalmic antibiotic (such as a triple-antibiotic formulation) to sterilize the corneal surface before the grid keratotomy is performed. The first stage in this therapeutic procedure is conveniently the final step required for diagnosis—removal of any redundant, nonadherent epithelium via débridement with a dry cotton-tipped applicator after corneal application of topical anesthetic. The epithelial lip surrounding indolent ulcers is very easily débrided, which sometimes results in an extensive ulcer. Occasionally, epithelium can be débrided out to the limbus over part or all of the corneal surface. This is, however, a necessary first step, and inadequate débridement is one of the more common reasons for treatment failure. A simple (nonindolent) ulcer cannot be débrided in this fashion.

Grid keratotomy is performed after débridement. General anesthesia or sedation is recommended for fractious dogs and for a clinician learning this technique. With compliant animals and an experienced operator, topical anesthesia and good restraint or sedation may be sufficient. Grid keratotomy consists of making linear striations in the cornea in a “cross-hatch” or grid pattern using the tip of a 25-gauge needle. A tuberculin syringe seems to make the ideal “handle” for directing the needle. Striations must extend from normal adherent epithe-

C D

FIGURE 10-32. Corneal débridement and grid keratotomy. A, After application of a topical anesthetic, all loose corneal epithelium is débrided with a cotton-tipped applicator in radial sweeps toward the limbus. B, A 25-gauge needle is dragged on a shallow angle and with its bevel up across the ulcerated cornea until a series of approximately parallel score marks has been made in the corneal stroma to a depth not exceeding 25% of the stroma; inset shows greater detail. C, A second set of stromal grooves is made at about 90 degrees to the first set. D, A therapeutic soft contact lens or biodegradable collagen shield can be placed over the ulcerated cornea. Note: This technique is contraindicated in feline corneas.

lium through the ulcer bed and must emerge in normal adherent epithelium on the other side of the ulcer. They must be multiple and deep enough to create obvious, visible score marks in the corneal stroma.

Medical therapy is continued afterward as for any superficial ulcer. A single postoperative dose of atropine is usually sufficient to control reflex uveitis. Hyperosmotic (5%) sodium chloride ointment is recommended if corneal edema is marked, because it might further decrease already impaired epithelial adhesion. Grid keratotomy may be combined with application of a soft contact lens and partial temporary tarsorrhaphy. This step provides greater protection for the healing cornea and contact lenses may increase surface tension via a gentle “suction-cup” effect, thereby enhancing epithelial adhesion. When a contact lens is in place, ophthalmic solutions rather than ointments should be used to ensure drug delivery to the corneal surface and to minimize chances of dislodging the contact lens. A success rate of approximately 80% can be expected with grid keratotomy alone. Treatment failures tend to arise when patients are “under-treated” by inadequate débridement or by making too few, too superficial, and/or too short score marks in the cornea. For indolent ulcers that have not healed 10 to 14 days after an initial grid keratotomy, the procedure should be repeated. Recurrent or unresolved cases should be referred for a superficial keratectomy.

Grid keratotomy is a potent treatment for indolent ulcers in dogs, but it is contraindicated in all other ulcer types in dogs and in ulcers in other species. The indolent ulcer diagnosis has not been proven to occur in cats or horses, and grid keratotomy is absolutely contraindicated in cats, in which it frequently induces a corneal sequestrum.

Grid keratotomy is the treatment of choice for indolent ulcers in dogs. It should NEVER be used in cats.

Epithelial Inclusion Cysts

Epithelial inclusion cysts are an uncommon sequela to corneal ulceration or trauma. They occur when epithelial cells become disorganized during healing such that they form small, epithelium-lined cysts that, with progression, become fluidfilled, yellow corneal masses (Figure 10-33). They protrude from the corneal surface and indent the stroma itself but are not

FIGURE 10-33. Corneal epithelial inclusion cyst. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

infected and cause little corneal reaction or pain. The cysts are removed with superficial keratectomy.

Mycotic Keratitis

Bacterial and viral infections of the cornea are much more commonly recognized than fungal infections in most parts of the world. However, particularly in tropical and subtropical areas, any corneal ulcer that does not respond to antibiotic therapy, especially one associated with stromal infiltration with white blood cells and especially in a horse, should be scraped. The exfoliated tissue should then be examined cytologically and cultured for possible mycotic involvement. Antifungal sensitivity testing can be done but is slow and expensive. There is also some controversy about the clinical applicability of in vitro sensitivity data. In a study of equine ulcerative keratomycosis in Florida, the frequency of fungal isolates was

Aspergillus, 41%; Fusarium, 32%; Penicillium, 9%; Cylindrocarpon, 4%; Scyalidium, 4%; Torulopsis, 4%; and yeast, 4%. The in vitro susceptibility of the isolates to different antifungal agents was natamycin = miconazole > itraconazole > ketoconazole. The organisms were significantly less susceptible to fluconazole than to the other medications. In a separate series of 35 fungal isolates from equine eyes, the following susceptibilities were reported: natamycin, 97%; nystatin, 74%; miconazole, 69%; amphotericin, 51%; 5-fluoro- cytosine, 49%; and ketoconazole, 31%. Such reports must be interpreted with caution, however, because frequency of different organisms shows geographic variation.

The clinical appearance of mycotic keratitis can also vary greatly. Generally, fungal infections have a much slower onset and course than bacterial infections as well as a classic history of having been resistant to conventional antibiotic therapy. Horses with keratomycosis may be presented with ulcerative keratitis or corneal abscessation underneath an intact epithelium (see later). Regardless, one of the more characteristic features is focal, creamy yellow, somewhat “fluffy” corneal opacities at the advancing edge of the lesion—so-called satellite lesions (Figure 10-34). These are sometimes characteristically deep within the corneal stroma or at the inner endothelial surface. Other clinical signs are as expected for corneal lesions and include blepharospasm, conjunctival and episcleral

FIGURE 10-34. Equine stromal keratomycosis. Note the “fluffy” stromal infiltrate as well as the associated diffuse corneal edema and deep and superficial corneal blood vessels. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

A

B

C

10-35. Cytologic specimen from a corneal scraping showing septate, branching fungal hyphae (A), a neutrophil (B), and some corneal epithelial cells (C). (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

hyperemia, epiphora, and corneal edema and neovascularization. Patients with keratomycosis often appear to have more pain than would be expected for a similarly severe bacterial keratitis. Diagnosis requires observation of fungal elements within samples submitted for cytology (Figure 10-35), culture, or histopathology.

A subpalpebral lavage tube is essential in severe cases owing to the pain as well as the frequency and number of medications needed. Medical therapy should include topical or systemic treatment with an antifungal drug. Commonly used topical agents are shown in Table 10-1. Systemically administered agents are discussed in Chapter 3. Some authors recommend treatment as infrequently as once or twice daily at first, especially if reflex uveitis is poorly controlled because rapid fungal death is alleged to incite a potent immune reaction and worsening uveitis. Control of secondary uveitis with flunixin meglumine, and of ciliary spasm with 1% atropine ophthalmic drops or ointment, is essential. Because most antifungal agents do not have antibacterial properties, topical application of a broad-spectrum antibiotic is also required if ulceration is present. If the cornea is malacic, serum should be applied topically for its anticollagenase properties. In many horses an early decision to surgically debulk the lesion will hasten healing time, reduce pain, lessen the chance of globe rupture, and permit the harvesting of diagnostic samples from deep in the cornea. Keratectomy of the lesion and surrounding stromal opacities, followed usually by placement of a conjunctival graft to cover and vascularize the stromal defect, is also an excellent choice. Referral for penetrating or posterior lamellar keratoplasty may be required for very deep lesions.

Stromal Abscess

Corneal stromal abscesses are believed to occur when small corneal puncture wounds allow bacteria or fungi to gain entrance to the stroma. The epithelium then rapidly heals over these sites, leaving the infectious organisms sequestered in the avascular cornea, where they can replicate and elicit a marked inflammatory response known as a corneal abscess. Stromal abscesses are seen most commonly in horses. They appear as focal yellowish white corneal opacities, with evidence of usually marked uveitis (Figure 10-36, A). Corneal vascularization is variable and is the means by which these lesions

ultimately heal if not surgically resected and treated with a corneal or conjunctival graft (Figure 10-36, B).

Etiologic diagnosis is challenging because the depth of these lesions within the cornea limits collection of samples to those obtained surgically during keratectomy. Likewise, penetration of antimicrobial agents is often limited by the intact epithelium overlying these abscesses. For these two reasons, referral for diagnosis and surgical treatment is recommended. Recently some success has been achieved with systemic administration of an antifungal agent such as fluconazole, which penetrates the blood-ocular barrier and achieves adequate concentrations in the aqueous humor (see Chapter 3).

Corneal Lacerations

Corneal lacerations occur commonly in all species. In dogs and cats they are frequently secondary to cat-scratch injuries. In horses sharp trauma from objects in the environment is most common. Blunt trauma also causes globe rupture; however, this tends to be along the limbus rather than dissecting across the central cornea. An attempt to differentiate blunt from sharp trauma is important because the former carries a greater risk of intraocular damage. Regardless of cause, three prognostic factors should be established in all corneal lacerations: depth of the laceration, involvement of the lens, and extension of the

FIGURE 10-37. Corneal laceration (A) and associated anterior lens capsule rupture (B). Owing to the elasticity of the anterior lens capsule, a simple linear laceration usually “gaps” open to become elliptical, as seen here. Note also the intralenticular melanin and iris from the neighboring iris. This appearance is strongly suggestive of lens capsule rupture. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

laceration beyond the limbus. Whenever possible, referral to an ophthalmologist is recommended.

Lacerations that penetrate the superficial corneal layers only, rather than the entire corneal thickness, usually have a good prognosis with appropriate care. They are treated in essentially the same way as ulcers. Perforating wounds with globe rupture have a poorer prognosis because of intraocular damage and greater tissue disruption at the wound edge. They heal by vascularization (either slowly and naturally from the limbus or prolapsed iris, or via a conjunctival graft). Regardless, there is more scar tissue and corneal opacification.

A careful examination is made to evaluate the extent of intraocular injuries. Great care must be taken to prevent pressure on the globe so as to avoid the risk of further intraocular damage. One of the most common causes of severe endophthalmitis and often secondary glaucoma leading to enucleation is unrecognized damage to the lens and its capsule from a perforating corneal injury (Figure 10-37). This damage causes phacoclastic uveitis that is usually unresponsive to medical treatment and may require emergency lensectomy (see Chapter 13). A careful assessment of the limbus for the full 360 degrees should be conducted. Lacerations that extend beyond the limbus carry a great risk of involvement of the underlying ciliary body and retina with marked uveitis, retinal detachment, and sometimes phthisis being likely. If a menace response cannot be elicited and the intraocular structures cannot be fully examined, a consensual pupillary light reflex from the affected to the normal eye should be evaluated. If major intraocular damage is evident, a consensual pupillary light reflex is present, and the limbus is intact, the patient should be referred for suturing of the corneal wound (Figure 10-38).

Removal of Corneal Foreign Bodies

Corneal foreign bodies are usually of two different types, those that adhere to the corneal surface by surface tension and may subsequently become even more firmly attached by creating an ulcerated region at their borders (Figure 10-39) and those that penetrate into the cornea and sometimes into the globe itself (Figure 10-40). They must be removed to limit

C D

FIGURE 10-38. Repair of a corneal laceration. A, Correctly placed corneal suture. B to D, Incorrectly placed sutures: B, Suture made too deep penetrates the anterior chamber. C, Suture made too superficial results in poor endothelial closure and persistent edema. D, Uneven suture bites lead to poor apposition of wound edges. (Modified from Slatter D [editor] [2003]: Textbook of Small Animal Surgery, Vol II, 3rd ed. Saunders, Philadelphia.)

FIGURE 10-39. Superficial, partially embedded corneal foreign body. This was a piece of plant material that could be forcibly rinsed from the corneal surface.

FIGURE 10-40. Penetrating plant material foreign body in a horse. This foreign body penetrated at the medial limbus and crossed the anterior chamber without penetrating or damaging the lens or iris. It required surgical removal.

pain, reduce the risk of infection, and prevent vascularization and scar formation. Small adhered foreign bodies are best removed with a fine stream of eye rinse or saline directed forcefully at the corneal surface after application of a topical anesthetic. This procedure is safe only if the cornea is not weakened, because a stream of fluid can rupture a descemetocele or other deep ulcer. Penetrating foreign bodies are more problematic and should be referred for surgical removal by means of an incision made in the cornea over the long axis of the foreign body under an operating microscope. After removal of either class of foreign body, a broad-spectrum topical antibiotic and atropine are administered to limit infection and the effects of secondary uveitis, respectively. If globe perforation has occurred, a systemically administered antibiotic should also be used. Corneal epithelial healing is normally rapid as long as secondary infection is controlled.

Keratoconjunctivitis Sicca

KCS is discussed in detail in Chapter 9.

Pigmentary Keratitis

Pigmentary keratitis is sometimes used as a clinical diagnosis when corneal melanosis is noted. In fact, corneal melanosis is simply a sign of chronic keratitis due to any number of causes, each with a different treatment and prognosis. Corneal melanosis (see Figure 10-12), its causes, and the diagnostic steps to follow when it is noted were previously described in the section on pathologic responses. The most common causes of corneal melanosis (and the chapters in which they are discussed) are as follows:

•Chronic exposure due to brachycephalic ocular syndrome (see Chapter 6)

•Cilia disorders (see Chapter 6)

•Tear film dysfunction (see Chapter 9)

•Any combination of the preceding conditions

Treatment is directed at halting progress of the melanosis through correction of the underlying cause. This usually stops further melanin deposition, but melanin already present may be slow to recede if it does so at all. For this reason, the importance of early detection of subtle melanosis and correction of causes before melanosis is advanced cannot be overstated.

“Pannus” or Chronic Immune-Mediated Superficial Keratoconjunctivitis

Pannus classically refers to nonspecific vascularization of avascular tissue (e.g., cartilage or cornea). However, it has been used so commonly to describe a characteristic immunemediated disease of the cornea and conjunctiva of dogs that it is also used here by common convention. Other synonyms that have been used are Uberreiter’s syndrome and chronic immune-mediated keratoconjunctivitis syndrome. Although a distinct breed predilection for this disorder is seen in German shepherds and greyhounds, it can affect any dog breed and should never be discounted as a diagnosis simply because the patient is not one of the commonly affected breeds.

The exact etiology is unknown. Cell-mediated immunity to corneal and uveal antigens has been demonstrated in affected corneas; however, this can also occur in many other chronic

inflammatory corneal disorders. Epidemiologic evidence of increased severity and greater resistance to treatment in patients residing more than 4000 feet above sea level suggests that ultraviolet radiation is important in the pathogenesis. It has been proposed that ultraviolet radiation alters the antigenicity of tissue in susceptible corneas, resulting in cell-mediated “auto-immunity.”

In the early stages, corneal epithelial cells proliferate and the superficial stroma is infiltrated by plasma cells and lymphocytes. As the disease progresses, melanocytes, histiocytes, and fibrocytes also enter the cornea, and edema and neovascularization occur. In the advanced stage, the corneal epithelium and anterior stroma become heavily melanotic and vascularized, and the epithelium may become keratinized (Figure 10-41). The epithelium remains intact in this disease, but frequently the mounds of fibrous granulation tissue retain fluorescein and the irregular corneal surface permit pooling of fluorescein. Both findings provide the illusion of ulceration. The syndrome tends to affect the temporal, nasal, inferior, and superior corneal quadrants, listed in descending order of occurrence and severity. Corneal vascularization and melanosis occur first at the temporal limbus and gradually move centrally. The other quadrants are gradually affected, and eventually the whole cornea may be involved. Edema and corneal degeneration often occur in the stroma 1 to 3 mm ahead of the advancing lesion. Depigmentation and thickening of the external surface of the third eyelid, usually near the margin, is common and can even occur without corneal lesions. This process contributes to the inflamed appearance of the eye. Mucoid ocular discharge is common.

The age of onset and breed of the affected animal are of prognostic significance. In animals affected when young (e.g., 1 to 2 years) the condition usually progresses to severe lesions, whereas animals first affected at a later age (e.g., 4 to 5 years) have less severe lesions. Severity of the disease also appears to vary with locality. Animals with higher sun exposure (because of latitude or elevation) show more severe lesions, which progress more rapidly to a more advanced state and respond to therapy less favorably, than do dogs with less ultraviolet exposure. Lesions must affect a large area of the cornea before vision is affected, and some cases may be quite advanced before first being noticed by the owner. Although the appearance of lesions is

10-41. “Pannus” (chronic immune-mediated keratoconjunctivitis syndrome) in a dog. Note the cobblestone-like plaque of granulation tissue and melanin over the lateral cornea with a leading band of corneal edema. The third eyelid is similarly affected, as is common in this syndrome. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

often characteristic, especially if noted in a predisposed breed with appropriate sun exposure, diagnosis can be confirmed by cytologic assessment of a corneoconjunctival scraping, which is usually almost purely lymphocytic/plasmacytic. Pannus must be distinguished from corneal melanosis due to other chronic irritation, such as KCS, exposure, and frictional irritation, as well as from granulation tissue present in vascular healing of corneal stromal wounds.

Pannus is a chronic progressive corneal disorder that cannot be cured. The therapeutic goal should be control and sometimes regression of the lesions so that blindness can be avoided. The owner must understand that lifelong therapy is necessary at a level depending on the severity in each patient and the geographic locality. With the exception of susceptible patients living at high elevation, useful vision can usually be preserved with medical therapy alone. In patients living at low elevation or for mild lesions occurring in middle-aged dogs, treatment consists of topical application of a potent and penetrating corticosteroid eyedrop, such as 0.1% dexamethasone or 1% prednisolone two to four times daily and/or topical cyclosporine (1% to 2%) twice daily until an adequate response is seen. Therapy can then be tapered as dictated by severity of signs. Improvement usually takes a minimum of 3 to 4 weeks to become apparent. The goal should be the minimum number and frequency of medications needed to prevent progression or recurrence. If possible, the corticosteroid should be stopped and the animal maintained on cyclosporine alone, as the latter has fewer side effects with long-term use. In severe or resistant cases, subconjunctival corticosteroids (preferably short-acting repository preparations with 7 to 14 days’ duration of action) may be necessary in addition to topical therapy.

Neurogenic Keratitis

Neurogenic keratitis is a collective term for neurotrophic keratitis due to loss of sensory innervation to the cornea (trigeminal nerve dysfunction) and neuroparalytic keratitis due to loss of motor innervation to the eyelids (facial nerve dysfunction). With neurotrophic keratitis, the corneal pathogenesis involves failure of the sensory stimulus to blink and protect the cornea as well as loss of the trophic factors supplied to the cornea via axoplasmic flow through the trigeminal nerve. There may also be associated masticatory muscle atrophy and enophthalmos. In neuroparalytic keratitis, interruption of motor innervation of the eyelids causes inadequate blink, lack of distribution of the precorneal tear film, and lack of protection of the corneal and conjunctival surfaces from friction and exposure. Instead of the normal blinking action of the upper and lower eyelids, the globe is often retracted, with subsequent passive movement of the third eyelid across the cornea.

Owing to anatomic position of the relevant nerves, neurotrophic keratitis tends to be associated with orbital disease, whereas neuroparalytic keratitis is seen most commonly in horses with guttural pouch disease and in other animals (especially dogs) with chronic otitis or after surgery for chronic otitis. In the early stages of both diseases, corneal epithelial degeneration and stromal edema occur. More advanced lesions include corneal desiccation and opacification due to vascularization and melanosis. Ulceration may occur with either form of neurogenic keratitis and may progress to perforation. Treatment involves temporary or permanent partial (usually

lateral) tarsorrhaphy (see Figure 10-29) to prevent corneal trauma and desiccation. Supplementation of the tear film is essential, and topical antibiotic therapy is necessary if corneal ulceration is present. Prognosis totally depends on the cause and treatment options for the primary condition causing the neurologic deficit. If treatment is not possible, enucleation may be required.

Feline Herpetic Keratitis

Feline herpesvirus type 1 (FHV-1) is a very common pathogen of the cornea and conjunctiva of the cat. Although the virus preferentially infects and replicates within the conjunctiva, it does commonly cause corneal disease. Only the corneal syndromes are discussed here. The reader is referred to Chapter 7 for a full discussion of relevant virology, pathogenesis, and conjunctival signs, along with methods of diagnosis and treatment. Feline herpesvirus may affect the corneal epithelium or stroma and produce different clinical entities in each. Epithelial replication results in severe ulcerative keratitis, which is dendritic at first (Figure 10-42) but rapidly becomes geographic (i.e., maplike). Disease within the corneal stroma is believed to result from viral particles or antigens entering through ulcerated epithelium and may result more from immunopathology than from viral replication. Both forms can occur in young kittens after primary infection or in adult cats as a result of reactivation of virus quiescent in sensory ganglia after periods of stress or administration of corticosteroids.

Herpetic keratitis in cats, like herpetic conjunctivitis, is frequently resistant to treatment, and relapses are common. Therapy usually involves topical use of antiviral agents, topical antibiotics if ulceration is present, and, sometimes, oral administration of lysine. Occasionally, surgical removal of the affected tissue by superficial keratectomy is also useful. The use of corticosteroids and cyclosporine is controversial and usually contraindicated, and these agents certainly should never be used without concurrent antiviral therapy and close clinical monitoring.

Corticosteroids are contraindicated in feline herpetic keratitis and should be used with caution in any feline eye because of the frequency of herpesvirus infection.

FIGURE 10-42. Dendritic corneal ulcers in a cat. These lesions are considered pathognomonic for feline herpesvirus infection. (Courtesy University of California, Davis, Veterinary Ophthalmology Service Collection.)

FIGURE 10-43. Feline eosinophilic keratoconjunctivitis. Note the raised chalky plaque in the dorsolateral cornea and the leading zone of corneal ulceration with dendritic margins. (From August JR [2001]: Consultations in Feline Internal Medicine, ed 4. Saunders, Philadelphia.)

FIGURE 10-44. Equine eosinophilic keratoconjunctivitis. Note the similarities in clinical appearance to feline eosinophilic keratitis as shown in Figure 10-43.

Feline Eosinophilic Keratoconjunctivitis

Feline eosinophilic keratitis (FEK) is an enigmatic disease of cats. Clinically, it appears as single or multiple focal, raised, pink plaque(s) resembling granulation tissue. Sometimes the plaques have a chalky appearance (Figure 10-43). Most cases are unilateral, but bilateral involvement is possible. Typically the lateral cornea is initially involved, but in advanced cases the entire cornea may be affected. Areas of corneal ulceration are also possible, particularly on the leading edge of the lesion. Third eyelid and/or conjunctival involvement is seen relatively commonly along with keratitis and occasionally alone. Eyelids can also be involved. Diagnosis is suggested by clinical appearance and confirmed with cytologic demonstration of eosinophils and mast cells along with neutrophils and hyperplastic or dysplastic epithelial cells. The cause is undetermined, but the condition appears to be due to an aberrant immune response. In many cases the antigenic stimulus is unrecognized; however, a recent investigation suggests that FHV-1 DNA can be detected in corneal samples from approximately 75% of cats with FEK.

This disease has traditionally been treated with topical corticosteroids and/or systemic megestrol acetate. However, recurrences are common with this protocol. Potential involvement of FHV-1 presents clinicians with a dilemma, because use of immunomodulatory drugs, especially topical corticosteroids, for treatment of an eye that is potentially infected with FHV-1 warrants caution. Some cases improve with antiviral medications alone, and so it appears wise to begin therapy with a topical antiviral agent only and to recheck the patient in a week or so. If there is improvement and the owner is compliant, continuation of this regimen may be all that is necessary. At the very least, antiviral treatment should be continued for as long as there is evidence of active viral replication and certainly while ulceration is present. More commonly, a form of immunomodulatory therapy must be added to the regimen. Topical corticosteroids may be used if no ulcers are present, but even then, reactivation of FHV-1 and/or ulcer formation may occur once corticosteroid therapy is begun. This problem has led to the recommendation of oral megestrol acetate for FEK. However, potential complications of its use, such as mammary hyperplasia, diabetes mellitus, and mammary neoplasia, should be explained to the animal’s owner. Early diagnosis and treatment as described of recurrences will limit the need for protracted therapy.

Equine Eosinophilic Keratoconjunctivitis

A disease similar in appearance and cytologic appearance to FEK is also recognized in horses (Figure 10-44). Like cats, horses affected with equine eosinophilic keratoconjunctivitis demonstrate blepharospasm, epiphora or sometimes more caseous mucoid discharge, chemosis, conjunctival hyperemia, and, often, a white corneoconjunctival plaque surrounded by a region of superficial corneal ulceration and vascularization. The lateral limbal area is most commonly affected, and patients may be unilaterally or, less commonly, bilaterally affected. As in cats, diagnosis is confirmed by demonstration of large numbers of eosinophils in corneal scrapings. Once infectious organisms, especially fungus, have been eliminated by cytologic examination and culture, treatment should be initiated with topical dexamethasone or prednisolone (usually with a broadspectrum antibiotic such as neomycin–bacitracin–polymyxin B) applied three or four times daily. In resistant lesions, superficial keratectomy may enhance healing and shorten the course of the disease.

Corneal Sequestration

Corneal sequestration is a corneal disease unique to the cat. Synonyms include feline corneal necrosis, corneal mummification, and keratitis nigrum. Although any cat can be affected, Persian, Burmese, Himalayan, and maybe Siamese cats appear to be more susceptible. The cause of the disease is unknown, but it usually occurs after chronic ulceration. As such, feline herpesvirus is frequently incriminated and can be detected in at least 50% of biopsy specimens from cats with this disease. Occasionally corneal sequestration is seen in cats with no previous history of ulcerative corneal disease. The clinical signs are classic, with the appearance of a focal amber to black, usually central corneal plaque surrounded by a broader area of superficial ulceration (Figure 10-45). These lesions tend to be painful, and blepharospasm and epiphora are expected. Depending on chronicity, sequestra are often accompanied by corneal vascularization, edema, and stromal white blood cell infiltration due to a foreign body reaction stimulated by the necrotic tissue. The black material is pigmented and necrotic cornea, not melanin.

The necrotic plaque sometimes sloughs without the need for surgical intervention. In such cases ongoing medical manage-