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48

Feline Corneal Sequestrum

6. What other procedures may be necessary to remove sequestra?

If the surgical site needs to be supported with additional tissues, the options are numerous. Conjunctival flaps (180-360° and pedicle), Tenon's free graft, sliding corneal conjunctival graft, corneal grafts, and surgical adhesives all do the job. If donor corneas are available, both full-thick- ness and lamellar keratoplasties give postsurgical results that have clear central corneas as do the sliding corneal-conjunctiva grafts. Leukomas are usually the sequelae of grafts from Tenon's capsule, flaps, and glues (Figs. 5-8).

Figure 5. Deep keratectomy of a central corneal sequestrum showing the incision extending away from the sequestrum into the conjunctiva.

Figure 6. The sequestrum is removed by lamellar undermining with a Martinez spatula. The corneal splitting is carried beyond the limbus into the conjunctiva.

Figure 7. The split corneal layers are repositioned to appose together into the void left by the excised sequestrum.

Feline Corneal Sequestrum

49

Figure 8. The sliding conjuncti- val-corneal graft is sutured to the adjacent cornea with 8-D Vicryl. Note the central cornea now has clear tissue, but the periphery of the graft is opaque from the conjunctiva.

7.Following the surgical procedure elected, is it necessary to medicate the eye topically?

Yes, most ophthalmologists prefer to medicate a corneal wound with a broad-spectrum an-

tibiotic. Culture and sensitivity tests from the surgical site should be submitted on all keratectomy cases. The results many times are negative, possibly because the patient has been on topical antibiotics presurgically. Those that have resulted in positive cultures have a high incidence of Mi- CroCOCClIS, which usually will respond to antibiotics, such as tobramycin (Tobrex) or ciprofloxacin (Ciloxan). Ointments are preferred mainly for their longevity. Allografts and heterografts should also be treated with 0.2% cyclosporine (Optimmune) twice a day for 3-6 months, depending on acceptance of the graft. In addition to the above, topical corticosteroids (dexamethasone) should be used for regression of neovascularization once the healing has taken place.

8. Should atropine be used postoperatively?

Initially, mydriasis is indicated, so a dose of 1% atropine preand postoperatively usually lasts 3-5 days. If atropine solution is used frequently and over days to weeks, the medication causes adverse effects that outweigh the desired effects.

9.If some pigment remains in the deep stroma after the keratectomy, is that bad?

The incomplete removal of the stromal pigment does not have adverse long-term consequences.

A faint tint of brown may be the worst remaining consequence, but the healing will progress.

10.Where does the pigment come from?

It is not known for sure. It may arise from the lacrimal gland or from the conjunctival flora.

The pigment, whatever its source, can be noted in the tears. It can stain the hairs around the eyes; it can be absorbed onto tissue paper; and, if you treat an ulcerated cornea with a soft contact lens, it will densely stain the contact. Attempts to identify the stain have proven the pigment to be a protein (Fig. 9).

11. In which cat breeds are sequestra most prevalent?

The breeds of highest incidence of sequestrum occurrence are the Burmese, Himalayan, and Persian. These breeds all have shallow orbits and protruding eyes, which make their corneas particularly vulnerable to microtrauma from trichiasis, entropion, lagophthalmia, and associated diseases of the adnexa.

12. Is there anything that can be done to prevent recurrence if the diagnosis of sequestration has been made and surgical treatment instigated?

Although there are no guarantees, it is helpful to start a topical antiviral at the first indication of corneal irritation and confirmation of an ulcerative process. Also, vaccines should be main-

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Feline Corneal Sequestrum

Figure 9. Contact lens removed from a postkeratectomized eat's cornea after only 2 days of placement. The pigment absorbed into the contact on the left with such affinity that it could not be washed away.

Figure 10. Champion Persian with unilateral sequestrum.

Figure 11. Champion Persian closeup of the left eye sequestrum shown in Figure 10.

tained faithfully to keep the titer high. Supplemental oral lysine can be considered. Antivirals can be used in conjunction with antibiotics. Even Champion Persians are susceptible (Figs. 10 and 11).

BIBLIOGRAPHY

I. Andrew SE, Tou S, Brooks D: Corneoconjunctival transposition for the treatment of feline corneal sequestra; A retrospective study of 17 cases (1990-1998). Vet OphthalmoI4:107-111, 2001.

2.Blogg JR, Stanley RG, Dutton AG: Use of conjunctival pedicle grafts in the management of feline keratitis nigrum. J Small Anim Pract 30:678-684, 1989.

3.Gimenez MTD, Farina 1M:Lamellar keratoplasty for the treatment offeline corneal sequestrum. Vet Oph-

thaimol I: 163-166, 1998.

Feline Corneal Sequestrum

51

4.Morgan RV: Feline corneal sequestration: A retrospective study of 42 cases (1987-1991). J Am Anim Hosp Assoc 30:24-28, 1994.

5.Nasisse MP, Guy JS, Davidson MG, et al: Experimental ocular herpesvirus infection in the cat. Invest Oph-

thaImol Vis Sci 30:1758-1768,1989.

6.Pentlarge VW: Corneal sequestration in cats. Comp Cont Educ Pract Vet 11:24-32,1989.

7.Schmidt GM, Whitley RD: Management of feline corneal sequestration: Medical therapy and surgical therapy. Vet Med Report 1:258-261, 1989.

8.Startup FG: Corneal necrosis and sequestration in the cat: a review and record of 100 cases. J Small Anim

Pract 29:476-286, 1988.

9. Wilkie DA, Whittaker G: Surgery of the cornea. Vet Clin N Am Small Anim Pract 27:1067-1107, 1997.

9. FELINE PROLIFERATIVE KERATOCONJUN CTIVITIS

Ronald C. Riis, D.v.M, M.S.

1.Is the feline species the only species to acquire proliferative keratoconjunctivitis?

No, the equine species also has a similar syndrome.

2.Have these syndromes been identified?

Collectively, they have been called eosinophilic keratitis.

3.Why is that term used?

The typical lesion is pink to white and is proliferative, from the surface of the cornea, con-

junctiva, or nictitans. It is irregular on the surface and in shape. Transillumination of the eye displays dense neovascularization reacting to the involved areas. If cytology is performed from the lesions that are whitish and raised, the cellular response has high numbers of eosinophils among a mixed population of other inflammatory cells (Figs. 1-5).

Figure l. Note the proliferations at the limbus. This is an early manifestation of the syndrome.

4. What factors might confuse the interpretation of the cytology of proliferative keratoconjunctivitis?

Inflammatory cells and high numbers of free rod-like bodies sometimes appear similar to rod bacteria. Comparing the intact numbers of eosinophils found with other cells will clarify whether

52

Feline Proliferative Keratoconjunctivitis

53

Figure 2. This pink thickening of the medial cornea is a rather smooth infiltration of proliferative keratitis.

Figure 3. The proliferative component of this keratoconjunctivitis looks severe, but complete resolution was obtained with treatment.

Figure 4. The appearance of this lesion is raised enough to rule oulin situ neoplasms, but cytology confirmed tremendous numbers of eosinophils. The response to treatment was excellent.

54

Feline Proliferative Keratoconjunctivitis

Figure S. Electron microscopy of feline proliferative keratopathy. The inflammatory cells on the surface are eosinophils with their characteristic cytoplasmic granules (7,ll7X).

Figure 6. Electron microscopy at the edge of a lesion of feline proliferative keratopathy. Epithelial degeneration with vacuolation at the basement membrane and stromal collagen disorganization (lIS,300X).

Feline Proliferative Keratoconjunctivitis

55

eosinophils have released their cytoplasmic granules. The slide preparation technique may cause this traumatic fracture of the cells; a gentle blotting or rolling of the material gathered usually yields more intact eosinophils.

5.Are the eye manifestations in any way related to the dermatologic syndromes?

No, the ocular lesion is unique.

6.Is there any consistency to ocular involvement or breeds involved?

Usually, the condition presents as a unilateral problem; however, it has been seen bilaterally.

Previously diagnosed cases can re-present with the opposite eye involved. There is no breed or sex predilection.

7. What is the etiology of proliferative keratoconjunctivitis?

The etiology is uncertain, however, one study found PCR-positive results against feline herpesvirus-I (FHV -1) in 76.3% of the surgical samples taken from proliferative lesions. To add to the uncertainty, this author has diagnosed and treated specific-pathogen free (SPF) cats with proliferative keratoconjunctivitis.

8.What is the treatment for proliferative keratoconjunctivitis?

The lesions respond to corticosteroids. Depending on how aggressive you choose to be, top-

ical, subconjunctival, and oral medications all are effective. If the cat is difficult to treat and the lesions are large, all three routes can be used. Initially, give 0.1 ml of 40 mg/ml of methylprednisolone (Depo-Medrol) subconjunctivally. Oral megestrol acetate should be prescribed: 5 mg/day for 1 week, then 5 mg/every other day for 1 week, then 5 mg/every third day for 2 weeks, and tapering off after 6 weeks. Minor lesions need to be treated only with the topical medication.

9.Are there concerns over the use of megestrol acetate?

Yes, owners should be warned about possible polydipsia-polyuria signs. Most cats lose these

adverse signs once the dose is reduced or stopped. Some weight gain has also been noted on Ovaban, which is now off the market.

10. Causing a flare-up of FHV is a concern with corticosteroids use. Do nonsteroidal antiinflammatories work?

Topical 0.1 % diclofenac, 0.03% flurbiprofen, 1.0% indomethacin, and 1.0% Suprefen all reduce the neovascularization and, therefore, slow the proliferative course of the disease. These medications need to be used 4-6 times per day for several months, but the results still may not be as good as with corticosteroids. Another drawback is that cats become tired of frequent, long-term eye medications, and their owners feel they cause a bonding loss with this ritual.

11.Can a different therapy approach be used other than corticosteroids?

Yes, immunomodulators have been used.

12.Which immunomodulator has worked?

Interferon alfa-2a has been successful when used at an oral dose of 1000 IUlday/week, fol-

lowed by no treatment for 1 week, then again back on medication. This alternating schedule is continued as necessary, but eventually the treatment is completely cancelled. In severe cases, oral interferon is supplemented with topical steroids.

13.How is the interferon prepared?

Interferon alfa-2a (Roferon-A Roche Pharmaceuticals) is sold in units containing 3 million

IU. Aliquots are made up with 10,000 IU/ml and dispensed with directions to give oral 0.1 ml (1000 IU)/day.

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Feline Proliferative Keratoconjunctivitis

14. Are there any adverse effects from interferon in cats?

The only reported side effect is a reduced white blood cell level, which returns once the interferon is stopped. The alternating weekly dose helps keep the white blood cell level.

BIBLIOGRAPHY

I. Bedford P, Cotchin E: An unusual chronic keratoconjunctivitis in the cat. J Small Anim Pract 24:85, 1983.

2.Larocea RD: Eosinophilic conjunctivitis, herpesvirus, and mast cell tumor of the third eyelid in a cat. Vet Ophthalmo13:221-225,2000.

3.Nasisse M, Luo H, Wang Y, et al: The role of feline herpesvirus-I (FHV-l) in the pathogenesis of corneal sequestration and eosinophilic keratitis. Proc Am Coli Vet OphthalrnoI27:80, 1996.

4.Pentlarge VW, Riis RC: Proliferative keratitis in a cat: a case report. JAm Anim Hosp Assoc 20:477, 1984.

5.Pentlarge V. Eosinophilic conjunctivitis in 5 cats. J Am Anim Hosp Assoc 27:21,1991.

6.Prasse K, Winston S: Cytology and histopathology offeline eosinophilic keratitis. Vet Comp Ophthalmol 6:74,1996.

10. KERATOCONJUNCTIVITIS SICCA

Seth A. Koch, V.M.D., M.M.Sc., and John Sykes, D.V.M.

1. What is Keratoconjunctivitis sicca (KCS)?

KCS (kerato means "cornea" and sicca means "dry") is a disease in which the primary lacrimal gland has, for a variety of reasons, stopped functioning. The primary lacrimal gland supplies the aqueous portion of the precorneal tear film.

2.Describe the portions of the precorneal tear film.

Of the three parts of the precorneal tear film, the aqueous layer is the most copious, the lipid

layer and the mucin layer are produced by the tarsal glands and the conjunctival goblet cells, respectively. The aqueous layer is responsible for causing KCS.

3.What is the primary lacrimal gland?

There are two lacrimal glands in the canine and feline. The primary lacrimal gland is located

at the lateral aspect of the upper lid (2-3 mm from the lid margin). The ducts of the lacrimal gland bathe the corneal surface. The secondary or accessory lacrimal gland, or gland of the third eyelid, is responsible for about 30% of the total aqueous tear production. This gland can be negligently or mistakenly removed when it becomes swollen ("cherry eye"). Removal of this gland may result in significant decrease in tear production. In susceptible patients (breed related), there will be a resultant "dry eye" syndrome. A number of accepted surgical techniques should be used to ensure appropriate cosmesis and continued function of the gland. For discussion of the various surgical techniques see Chapter 12.

4. Which breeds are susceptible to KCS?

A number of breeds are disproportionately affected with KCS. The English bulldog, cocker spaniel, Pekingese, West Highland white terrier, schnauzer, and Yorkshire terrier are the most common breeds observed with the syndrome. The Yorkshire terrier has been reported to have congenital acinar hypoplasia as a genetic defect, and KCS is, therefore, seen in the young "Yorkie."

5.What are the clinical findings of KCS?

As with many other ocular irritative diseases involving the conjunctiva and cornea, the pa-

tient will exhibit discomfort, photophobia (discomfort in bright light), blepharospasm (blinking), copious ropey mucopurulent discharge, crusting of the lid margins, corneal neovascularization, ulcers, and keratinization (pigment deposition) (Figs. I and 2).

6. This sounds just like a conjunctivitis. Where's the sicca?

The sicca part of the KCS is what makes the diagnosis of the disease definitive. Any case of conjunctivitis seen in practice should have a Schirmer tear test performed to distinguish KCS from the other conjunctivitides.

7.What is the Schirmer tear test?

The tear test is a piece of filter paper of a specific type that is usually dye-impregnated for

ease of reading. The strip of paper is bent at the indicated crease and inserted into the inferior conjunctival cul-de-sac at the lid margin. The amount of wetting that occurs in I minute is the recorded result. The conjunctival cul-de-sac should be cleansed with a dry cotton-tipped applicator to remove the debris prior to doing the test.

8.What's a normal reading for the Schirmer tear test?

Using the dye-impregnated strips, a finding of 12-15 mm of wetting in 1 minute is consid-

ered normal.

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