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

necessary. In some areas this “summer conjunctivitis” is due to release of Habronema larvae by feeding flies.

Immune-Mediated Conjunctivitis

Because of the conjunctiva’s exposed position and resident lymphoid tissue, immunopathology may occasionally initiate and often exacerbates conjunctivitis. In this chapter, the terms “immune-mediated” and “autoimmune” are not used interchangeably as is sometimes the case. Rather, disease caused by an autoimmune response form a subgroup of the broader immune-mediated group of diseases—that is, they are immunemediated disease in which the antigen is identified and is an autoantigen. Four reasonably common examples of conjunctival immunopathology are seen in small animal and equine practice: nodular granulomatous episclerokeratoconjunctivitis, allergic conjunctivitis, eosinophilic keratoconjunctivitis, and pannus (or chronic superficial keratoconjunctivitis). Because all except allergic conjunctivitis typically produce more overt signs of keratitis than of conjunctivitis, they are described in Chapter 10. Allergic conjunctivitis is discussed here.

Allergic Conjunctivitis

Allergic conjunctivitis can occur after exposure of the conjunctiva to antigens as a result of direct contact (airborne or topically applied agents), inhalation, or ingestion and may be seen with signs of more widespread atopy or allergic responses. The response is elicited by many different kinds of antigens and can occur in all species. The clinical signs are as follows:

•Periocular erythema and conjunctival hyperemia (Figure 7-10)

•Serous to mucoid discharge

•Chemosis

•Concurrent inflammation of the skin, paws, nasal cavity, ears, or pharynx

As with all other forms of conjunctivitis, achieving an etiologic diagnosis is essential. Trials whereby potential antigens are removed from and then reintroduced to the animal’s environment are useful. However, it is most important to eliminate other, more common causes of conjunctivitis. Therefore a Schirmer tear test should always be performed to eliminate keratoconjunctivitis sicca. Conjunctival cytology is important in the accurate diagnosis of allergic conjunctivitis. Eosinophils are not always present, but lymphocytes and

plasma cells are frequently seen. Secondary bacterial conjunctivitis may occur after inflammation has been initiated by an antigen. Toxins produced by bacteria (e.g., S. aureus) present in the conjunctival sac or meibomian glands may also initiate allergic conjunctivitis, but the clinical appearance differs from that of spontaneous or atopic conjunctivitis. Food allergy also results in allergic conjunctivitis in calves. Hypersensitivity to medications such as neomycin and other aminoglycosides may occur.

Treatment of Immune-Mediated Conjunctivitis

1.Topical corticosteroid therapy at a frequency and concentration as low as possible to control (but usually not cure) the condition is the mainstay of therapy. In mild cases, a low-potency corticosteroid such as hydrocortisone may be used intermittently. More commonly, especially early in the disease course, topical application of a more potent, penetrating corticosteroid such as dexamethasone or prednisolone is required.

2.Topical application of cyclosporine has been used for some time to treat immune-mediated conjunctivitis in dogs and is now under investigation for vernal conjunctivitis in humans.

3.Mast cell–stabilizing agents and antihistamines have been used topically to treat allergic and eosinophilic conjunctivitis. However, anecdotal reports of the efficacy of these products vary, and controlled studies on their safety or efficacy in veterinary patients are lacking.

4.Local antibiotic preparations may help in the short term if secondary bacterial conjunctivitis is present. However, many antibiotics (such as neomycin) can cause allergic conjunctivitis. Although this drawback is insufficient to prevent their routine use, it should be considered if the conjunctivitis worsens when a new drug is begun.

5.Systemic therapy with corticosteroids, more potent immunosuppressive agents, antihistamines, antibiotics, and hyposensitization therapy may be required in severe cases with skin (including eyelid) involvement.

OTHER CONJUNCTIVAL DISORDERS

Drug Plaques

Certain repository medications (e.g., methylprednisolone) leave unsightly, creamy-white subconjunctival plaques months after injection in some animals (Figure 7-11). The material in these plaques may also incite a local granulomatous conjunctivitis around the material. In such cases surgical excision is required.

Conjunctival Lacerations

Traumatic lacerations of the conjunctiva heal very rapidly, and small lacerations usually require only short-term topical antibiotic therapy. More severe lacerations are flushed with saline to remove foreign material, sutured with 6/0 or 7/0 polyglactin 910 (Vicryl) or polydioxanone (PDS) suture, and treated with topical antibiotics.

FIGURE 7-10. Allergic dermatitis (blepharitis) and conjunctivitis. (From Muller GH, Kirk RW [1989]: Small Animal Dermatology, 4th ed. Saunders, Philadelphia.)

Ligneous conjunctivitis is a chronic, membranous conjunctivitis with gross thickening of palpebral and third eyelid con-

FIGURE 7-11. Plaque formation following subconjunctival injection in the dorsal bulbar conjunctiva of a dog.

junctivae bilaterally (Figure 7-12). There is some evidence that younger, female Doberman pinschers may be predisposed. A conjunctival biopsy should be performed to confirm the diagnosis. Histology demonstrates a characteristic amorphous, eosinophilic hyaline material throughout the subconjunctiva. In some animals, other mucous membranes may also be involved and most dogs have evidence of nonocular disease, especially involving the upper respiratory or urinary tract. A vascular basis for the disease is proposed. Topically administered cyclosporine is often effective at controlling the disease, although systemic administration of immunomodulatory agents may be necessary, and recurrence is relatively common.

Lipogranulomatous Conjunctivitis

Lipogranulomatous conjunctivitis has been described in cats. It is an inflammatory condition that arises from the meibomian glands and therefore manifests superficially as blepharitis and on the inner eyelid surface as a nodular conjunctivitis (Figure 7-13). Involvement of multiple tarsal glands across one or more eyelids, producing a multifocal nodular white thickening of involved lids, is common. The upper eyelid is involved more commonly than the lower lid. Actinic radiation may be important in the pathogenesis of these lesions because they have been reported more commonly in white-skinned cats and sometimes

FIGURE 7-12. Ligneous conjunctivitis in a dog. (Courtesy Dr. David Ramsey.)

FIGURE 7-13. Lipogranulomatous conjunctivitis of the upper eyelid of a 16-year-old domestic cat. (From Read RA, Lucas J [2001]: Lipogranulomatous conjunctivitis: clinical findings from 21 eyes in 13 cats. Vet Ophthalmol 4:93.)

in association with squamous cell carcinoma (SCC). If meibomian glands rupture, secretions leak into the surrounding tissue and cause a marked lipogranulomatous reaction. Histologic appearance is similar to that of chalazia in dogs (see Chapter 6).

Surgical extirpation of glandular material and associated granulomatous infiltrate has been recommended for this condition. A conjunctival approach is preferred because of the rapidity with which conjunctiva heals and to avoid surgical disruption of the eyelid margin. Surgical treatment involves resection of lipogranulomas and overlying conjunctiva as a single strip of tissue outlined by two incisions parallel to the eyelid margin. The defect is allowed to heal without suturing.

Conjunctival Neoplasia

Neoplasia of the conjunctiva may occur in any species and may represent primary or metastatic disease. Of the conjunctival neoplasms, SCC is the most common. Others commonly recorded are hemangioma and hemangiosarcoma, melanoma, papilloma, and mastocytoma. As with masses elsewhere, cytologic assessment of scrapings or aspirates, or histologic assessment of biopsy specimens is essential for accurate diagnosis because neoplastic and nonneoplastic masses may appear similar on clinical examination alone. Involvement of neighboring eyelids, cornea, or sclera is common, and the reader is referred also to chapters dealing with these tissues for additional information.

Conjunctival Dermoid

Dermoids are examples of a choristoma or congenital circumscribed overgrowth of microscopically normal tissue in an abnormal place. Conjunctival dermoids represent histologically normal skin arising in the conjunctiva, usually laterally, and frequently involving the limbus (Figure 7-14). Dermoids occasionally involve the eyelids and may coexist with an eyelid coloboma. Dermoids containing hair follicles have hair growing from the surface, which causes conjunctival and corneal irritation

FIGURE 7-14. A conjunctival dermoid with obvious tufts of irritating hairs in a 6-month-old shih tzu.

and leads to epiphora and keratitis. Dermoids usually grow slowly, if at all. In Hereford cattle they are inherited, with recessive and polygenic genetic characteristics being reported.

Treatment for dermoid is careful surgical excision via conjunctivectomy and dissection down to bare sclera. If the lesion extends onto the cornea, referral to an ophthalmologist for combined conjunctivectomy and keratectomy is recommended.

Ocular Squamous Cell Carcinoma

SCC is probably the most common conjunctival neoplasm in veterinary medicine. It is regularly seen in horses, cattle, small ruminants, and cats but occurs very infrequently in dogs. Some general comments regarding clinical signs, progression, malignancy, diagnosis, and therapy are possible. Some specific comments regarding this tumor in cattle are found in the next section.

ETIOLOGY. The exact etiology is unknown. However, incidence of SCC is much higher in animals with hypopigmentation and in areas of high sunlight or altitude, in which exposure to ultraviolet radiation is greater. About 75% of cases in cattle occur in animals lacking pigment in the eyelids, third eyelid, or conjunctiva. Therefore selection for lid pigmentation has been used as a control measure in cattle. Lid pigmentation is highly heritable and is present at birth, whereas conjunctival pigmentation has a lower heritability and develops throughout life. Although viral particles have been demonstrated in SCC lesions, an etiologic relationship has not been established.

CLINICAL SIGNS AND PATHOGENESIS. For the globe (conjunctiva, cornea, and limbus) and third eyelid, plaque is the initial precursor lesion of SCC (Figure 7-15). Plaques are grayish-white areas of thickened epithelium occurring most frequently at the nasal and temporal limbus. On the lids, the precursor lesion is the keratoma, a brown, crusty, and sometimes hornlike structure, that occurs at mucocutaneous junctions (Figure 7-16). Papilloma is the next stage and has a similar distribution, but the surface is roughened and the mass is frequently pedunculated or moveable. The base often merges with an underlying plaque. Carcinoma in situ may arise from any of these lesions. This term is used for the stage before the neoplastic cells have penetrated the basement membrane of the epithelium and entered the subepithelial connective tissue to become true

SCC

FIGURE 7-15. Pathogenesis of bovine squamous cell carcinoma (SCC) at various ocular sites.

7-16. Eyelid keratoma on the lower eyelid of a cow. This is a precursor lesion for squamous cell carcinoma. (Courtesy Dr. David Ramsey.)

FIGURE 7-17. Corneoscleral limbal squamous cell carcinoma in a cow.

SCC. The surface of carcinomas may be roughened or papillary, hemorrhagic, or ulcerated. (Figure 7-17).

The tumor is often aggressively invasive locally and may involve eyelids, intraorbital space and tissues, and even bone and paranasal sinuses. Metastasis is less common and typically involves local lymph nodes. The rate of progression of SCC is variable, with lesions ranging from slow-growing to highly malignant. Both cell-mediated and humoral immunity to tumor antigens has been demonstrated.

DIFFERENTIAL DIAGNOSIS. SCC must be distinguished from the following conditions:

•Other neoplastic lesions of the conjunctiva, including but not limited to melanoma (which can be poorly pigmented), lymphangiosarcoma, hemangioma, hemangiosarcoma, dermoid (which are not always haired), and lymphoma

•Granulation tissue, as seen with any chronic inflammatory process but especially pannus of dogs, eosinophilic keratoconjunctivitis of horses and cats, and chronic ulceration of any species but especially infectious bovine keratoconjunctivitis in ruminants. Differentiation of granulation tissue from SCC is particularly challenging when it occurs after resection of SCC when it may be mistaken for early tumor recurrence.

Biopsy or cytologic scraping (see Figure 7-6, J) of suspicious lesions is indicated and usually diagnostic, with up to 90% accuracy having been reported.

TREATMENT. Treatment depends on species, tumor location, value of the animal, and stage of the disease. Treatment options include surgical excision or debulking, cryotherapy, hyperthermia, immunotherapy, radiation therapy (numerous types), intralesional chemotherapy, and photodynamic therapy (see Chapter 3). Cryotherapy has the advantages of simplicity and rapidity, economy, analgesia, minimal preoperative and postoperative treatment, repeatability, and minimal side effects. Economic and radiologic health considerations may limit the use of radiotherapy.

Bovine Ocular Squamous Cell Carcinoma

INCIDENCE. SCC of the eye and adnexa is one of the most common and most important ocular conditions affecting cattle. It is uncommon in breeds with pigmented conjunctiva and lids but may occur in any breed. Herefords are affected most frequently (incidence may reach 10%), but SCC also occurs in shorthorn and Friesian cattle. Both the precursors to SCC and the disease itself are usually unilateral (10% are bilateral). Ocular lesions outnumber lid lesions by a ratio of 3:1, whereas lesions of the third eyelid account for less than 5% of the total lesions. Precursor lesions are not uncommon in animals younger than 4 years, whereas SCC is more common at 7 to 9 years and is rare before 5 years. Fifty percent of precursor lesions manifesting at the end of one summer may disappear by the next summer.

TREATMENT. In a large study of cryotherapy using a double freeze-thaw cycle to –25° C, an overall cure rate of 97% was achieved, and even quite large lesions responded well. Treatment with bacille Calmette-Guérin (BCG) cell wall vaccine injected into the tumor caused regression in 71% of affected animals. Intratumoral injection of 200,000 units of interleukin (IL-2) resulted in a 67% complete regression at 20 months after injection.

CONTROL. Incidence of ocular SCC within a herd may be reduced by selective breeding for lid, limbal, and conjunctival pigmentation, which are genetically related and heritable. Use of breeding animals whose progeny have not demonstrated SCC is also recommended because genetic factors other than periocular pigmentation are believed to be involved.

Canine Conjunctival Papillomatosis

Papillomas usually occur on the eyelids or mucocutaneous junctions and may be multiple, especially in young animals. For those arising from the conjunctiva, the most important differential diagnosis is SCC. The relationship to oral and

cutaneous papillomatosis is not established. Surgical removal or cryotherapy is the treatment of choice, especially if the lesion is causing pain from friction. Recurrence has been observed. Spontaneous regression of ocular papillomas occurs, especially in young animals.

Equine Conjunctival Angiosarcoma

Conjunctival angiosarcomas occur in aged horses, grow slowly, and metastasize despite excision and radiation therapy. They must be differentiated from SCC by biopsy. Enucleation may be necessary because these tumors are often very aggressive.

BIBLIOGRAPHY

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Bentz BG, et al. (2006): Pharmacokinetics of acyclovir after single intravenous and oral administration to adult horses. J Vet Intern Med 20:589.

Bonney CH, et al. (1980): Papillomatosis of conjunctiva and adnexa in dogs. J Am Vet Med Assoc 176:48.

Browning GF (2004): Is Chlamydophila felis a significant zoonotic pathogen? Aust Vet J 82:695.

Collins BK, et al. (1993): Biologic behavior and histologic characteristics of canine conjunctival melanoma. Prog Vet Comp Ophthalmol 3:135.

Garre B, et al. (2007): In vitro susceptibility of six isolates of equine herpesvirus 1 to acyclovir, ganciclovir, cidofovir, adefovir, PMEDAP and foscarnet. Vet Microbiol (in press).

Hacker DV, et al. (1986): Ocular angiosarcoma in four horses. J Am Vet Med Assoc 189:200.

Johnson BW, et al. (1988): Conjunctival mast cell tumors in two dogs. J Am Anim Hosp Assoc 24:439.

Haesebrouck F, at al. (1991): Incidence and significance of isolation of Mycoplasma felis from conjunctival swabs of cats. Vet Microbiol 26:95.

Lavach JD, et al. (1977): Cytology of normal and inflamed conjunctivas in dogs and cats. J Am Vet Med Assoc 170:722.

Longbottom D, Coulter LJ (2003): Animal chlamydioses and zoonotic implications. J Comp Pathol 128:217.

Maggs DJ (2005): Update on pathogenesis, diagnosis, and treatment of feline herpesvirus type 1. Clin Tech Small Anim Pract 20:94.

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Mughannam AJ, et al. (1997): Conjunctival vascular tumors in six dogs. Vet Comp Ophthalmol 7:56.

Nasisse MP, et al. (1997): Effects of valacyclovir in cats infected with feline herpesvirus 1. Am J Vet Res 58:1141.

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Ramsey DT, et al. (1996): Ligneous conjunctivitis in four Doberman pinschers. J Am Anim Hosp Assoc 32:439.

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Stiles J, et al. (2002): Effect of oral administration of L-lysine on conjunctivitis caused by feline herpesvirus in cats. Am J Vet Res 63:99.

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ocular disease. Am J Vet Res 64:1421.

ANATOMY AND PHYSIOLOGY

The third eyelid (or nictitating membrane) is a mobile, protective, and glandular structure lying between the cornea and the lower eyelid in the medial portion of the inferior conjunctival sac (Figure 8-1).

The third eyelid (Figure 8-2) consists of the following:

•A T-shaped cartilaginous “skeleton”

•The gland of the third eyelid

•Conjunctiva covering the bulbar and palpebral surfaces

•Numerous superficial lymphoid follicles under the bulbar surface

The T cartilage provides essential rigidity to the third eyelid. Its “horizontal” arm lies parallel to and about 1.5 mm from the leading edge of the third eyelid. The “vertical” arm runs perpendicular to the free edge and at its base is encircled by the gland of the third eyelid (see Figure 8-2). The gland of the third eyelid is seromucoid and produces up to 50% of the normal tear film in dogs. In the dog, this gland has both adrenergic and cholinergic innervation, with cholinergic being the denser. In the pig and many rodents a portion of the gland of the third eyelid or a separate gland (the Harderian gland) is found deeper within the orbit. The cartilage and gland are covered on both bulbar and palpebral surfaces by conjunctiva that is tightly adherent at the free margin of the third eyelid but looser over the base and gland. The free margin and a portion of the anterior face of the third eyelid are often but not always pigmented. Lymphoid follicles, which are pinkish red, are normally present beneath the conjunctiva on the bulbar surface of the third eyelid (Figure 8-3).

A poorly defined fascial retinaculum secures the base of the gland and the cartilage to the periorbita surrounding the ventral oblique and rectus muscles. The musculature controlling the third eyelid is largely vestigial in domestic species, and the membrane moves passively across the eye when the globe is retracted by the retractor bulbi muscles innervated by the abducens nerve. Movement is in a dorsolateral direction, toward the orbital ligament. The position of the third eyelid is also partially determined by sympathetic tone of the orbital smooth muscles. Interruption of this sympathetic supply, as in Horner’s syndrome, results in enophthalmos (posterior displacement of the globe within the orbit) and prominence of the third eyelid.

In birds the third eyelid is almost transparent and is under voluntary control (Figure 8-4). It sweeps over the globe in a ventromedial direction from the dorsolateral quadrant, although there is some species variation in direction of move-

ment. The third eyelid in birds does not have a gland associated with it.

The third eyelid has the following important functions:

•Distribution of the precorneal tear film

•Protection of the cornea

•Production of aqueous and immunoglobulin for the tear film (in domestic mammals)

Therefore removal of the third eyelid or its gland predisposes to the following problems:

•Increased corneal exposure, drying of the cornea, corneal trauma, and chronic keratitis

•A chronic conjunctivitis that is often purulent and frequently resistant to treatment

•Decreased tear production, which contributes to the first two problems

The third eyelid is a useful and important structure. The only indications for its removal are severe, irreparable trauma and histologically confirmed malignant neoplasia.

EXAMINATION

The clinician can easily examine the palpebral surface of the third eyelid by digitally retropulsing the globe through the upper lid. The bulbar surface is examined after application of topical anesthesia and the use of forceps or mosquito hemostats to grasp the leading edge of the third eyelid just outside the horizontal arm of the cartilage. The membrane can then be reflected to examine the bulbar surface and the space between the third eyelid and the globe (see Figure 8-3). This is a common site for foreign bodies to become lodged. The bulbar surface is normally follicular and may become more so with socalled follicular conjunctivitis (see Chapter 7).

Perhaps the most common abnormality of the third eyelid noted during an ocular examination is unusual prominence. This sign is seen with a number of third eyelid diseases discussed in this chapter. However, prominence of the third eyelid can also indicate other orbital, neurologic, or ocular diseases, which are discussed elsewhere; they include the following:

•Horner’s syndrome (sympathetic denervation)

•Third eyelid protrusion (or “haws”) syndrome

•Space-occupying orbital lesions that push the membrane across the eye from its base

FIGURE 8-1. Diagram of the eye showing normal position of the third eyelid. (Modified from Evans HE [1993]: Miller’s Anatomy of the Dog, 3rd ed. Saunders, Philadelphia.)

Iris

Sclera

Lateral

canthUs BUlBar sUrface of third eyelid

PUpil

Lymphoid tissUe

FIGURE 8-3. Diagram of the third eyelid manually everted to show normal lymphoid follicles on the bulbar surface. (Modified from Evans HE [1993]: Miller’s Anatomy of the Dog, 3rd ed. Saunders, Philadelphia.)

•With a small globe due to microphthalmos or phthisis bulbi

•With enophthalmos due to active retraction of the globe in painful ocular conditions or due to loss of orbital contents as in dehydration, atrophy, or fibrosis

•With tetanus, especially in large animals

•Tranquilization (e.g., with acetylpromazine)

DISEASES OF THE THIRD EYELID

Because the third eyelid has two surfaces of conjunctiva and is intimately associated and confluent with the rest of the conjunctiva, it is predictably involved in many conjunctival disorders. These are discussed more fully in Chapter 7. This chapter emphasizes conditions peculiar to the third eyelid.

Amelanotic Leading Edge of the Third Eyelid

Congenital absence of melanin on the free or leading edge of the third eyelid in some individuals reveals normal, well-vascularized conjunctiva, which is frequently mistaken by owners or breeders for third eyelid protrusion or inflammation. This appearance is not abnormal, however, and does not require surgical correction.

FIGURE 8-4. Third eyelid of a peregrine falcon showing translucency and voluntary dorsal-to-ventral movement typical of the avian third eyelid.

When such eyes become inflamed for other reasons, the amelanotic third eyelid may appear more visible because the conjunctival vasculature is not obscured by pigment. Also, such eyelids are presumed to be at higher risk for solar-induced neoplasms, such as hemangioma, hemangiosarcoma, and squamous cell carcinoma.

Eversion or Scrolling of the Third Eyelid

Eversion of the third eyelid or “scrolled third eyelid” refers to rolling out of the margin of the membrane due to abnormal curvature of the vertical portion of the T-shaped cartilage (Figure 8-5). This condition may be unilateral or bilateral, and although most commonly seen in young dogs, it occasionally develops in middle-aged dogs. It is common in Weimaraners, Saint Bernards, Newfoundlands, Great Danes, German shorthaired pointers, and Irish setters, and a hereditary basis has been suggested. Injuries and improper suturing of the third eyelid may also result in eversion.

Treatment

Eversion of the third eyelid is corrected surgically because of its undesirable cosmetic appearance and the resultant secondary conjunctivitis and keratitis in some animals. The deformed or buckled section of excessive cartilage is removed via a surgical approach from the bulbar surface (Figure 8-6). The

A

B

C

FIGURE 8-6. Surgical correction of third eyelid cartilage eversion. A, On the bulbar side of the third eyelid, the conjunctiva is incised overlying each side of the scrolled vertical part of the third eyelid cartilage. B, The scrolled cartilage and overlying conjunctiva are undermined with tenotomy scissors. C, The undermined section of scrolled cartilage and overlying conjunctiva is resected. No sutures are required.

defective, scrolled portion of cartilage is usually found in the vertical arm of the cartilage, near its junction with the horizontal arm of the T. A topical antibiotic ointment should be used for approximately 1 week after surgery.

Protrusion of the Gland of the Third Eyelid

Protrusion of the gland of the third eyelid (or “cherry eye”) occurs most commonly in dogs and occasionally in cats. The appearance is characteristic, with the gland of the third eyelid protruding as a reddish follicular mass from behind a usually “floppy” margin of the third eyelid (Figure 8-7). It likely results from lymphoid hyperplasia (in young animals exposed to environmental antigens for the first time) and laxity of the retinaculum that should attach the third eyelid to the periorbita (in genetically predisposed, especially brachycephalic, animals). This combination of events allows the gland to evert while remaining attached to the cartilage of the third eyelid.

The gland should be surgically replaced to retain essential lacrimal function and to prevent the exposed gland and overlying conjunctiva from becoming dry, inflamed, secondarily infected, and cosmetically unappealing. Prolapsed glands of the third eyelid should never be removed because the gland of the third eyelid is a significant contributor to precorneal tear film production. Studies confirm clinical experience that keratoconjunctivitis sicca is commonly seen, often years later, in animals, especially those of susceptible breeds in which the third eyelid or its gland was removed. Also, complications have been reported in prolapsed glands left in the prolapsed position.

Treatment

Occasionally in the early stages, a prolapsed gland can be manipulated into its normal position. However, recurrence is almost inevitable. For these reasons surgical replacement is practiced. If the gland is severely inflamed or the conjunctival surface secondarily infected, preoperative treatment for a few days with a topical antibiotic-steroid ointment is advisable; however, this treatment will not result in resolution of protrusion.

Corrective surgical procedures may be broadly categorized as “anchoring” or “pocket” techniques. The original anchoring method involved suturing the gland to the ventral aspect of the globe. This had a relatively high rate of recurrence owing to difficulty accessing and suturing to the sclera, and too frequently resulted in globe penetration during suturing. Therefore it is no

longer recommended. Numerous variations of the anchoring techniques have been proposed, with one of the methods in which the gland is sutured to the periosteum of the ventral orbital margin now being preferred (Figure 8-8). This procedure is associated with some reduction in third eyelid mobility. As a result, pocket techniques may be more physiologic. Of the pocket techniques, the technique of Morgan is very useful (Figure 8-9). Medical treatment after any replacement technique includes topical antibiotic-steroid ointment or solution and use of an Elizabethan collar. Oral administration of a nonsteroidal antiinflammatory agent may be indicated for postoperative analgesia. Recurrence is possible, even with a correctly performed pocket or anchoring technique, especially in the very large breed dogs such as mastiffs and Newfoundlands.

Prolapsed glands of the third eyelid are treated by replacement, NOT by excision.

Protrusion of the harderian gland occurs in dwarf lop rabbits with clinical signs and sequelae similar to those of third eyelid gland protrusion in dogs and cats. Replacement of the gland by anchoring to the orbital rim is recommended.

B

A

FIGURE 8-9. Surgical replacement of a prolapsed gland of the third eyelid (“cherry eye”) via a modification of the conjunctival pocket technique of Morgan. A, Two semielliptical incisions are made through the bulbar conjunctiva around the periphery of the prolapsed gland. The outer (free) edges of conjunctiva created by these incision are then apposed over the prolapsed gland using 4/0 to 6/0 absorbable suture, such as polyglactin 910 (Vicryl) in a simple continuous pattern. The initial and final anchoring knots are placed on the anterior face of the third eyelid to avoid frictional irritation of the cornea. B, The second (Cushing) layer of a continuous Connell-Cushing pattern is then placed with bites parallel to the conjunctival incisions, and, again, knots are placed on the anterior face of the third eyelid.

FIGURE 8-13. Adenocarcinoma of the third eyelid gland in a dog.

Larger tumors necessitate complete excision of the third eyelid and surrounding conjunctiva (Figure 8-15).

TRAUMA TO THE THIRD EYELID

Injuries to the third eyelid occur as a result of fights, motor vehicle accidents, and foreign body penetration. Usually, tears involving the conjunctiva only do not require suturing. Small

flaps off the leading edge can be safely removed. Larger lacerations, especially those involving the free margin and creating larger loose flaps, may benefit from careful appositional suturing with knots placed on the anterior surface so as to avoid frictional irritation of the cornea (Figure 8-16). Although some retraction takes place during healing, a functional third eyelid can often be retained. In some circumstances grafting of oral mucous membrane may be useful for replacing large defects.

INFLAMMATORY DISORDERS OF THE THIRD EYELID

The third eyelid is predictably involved in most conjunctival disorders. These are discussed more fully in Chapter 7. The third eyelid can be involved more obviously than or, rarely, to the exclusion of other conjunctival surfaces in so-called atypical pannus (see Chapter 10), eosinophilic keratoconjunctivitis of cats and horses (see Chapter 10), ligneous conjunctivitis of dogs (see Chapter 7), habronemiasis of horses (see Chapter 7), and nodular granulomatous episclerokeratoconjunctivitis of dogs (see Chapter 10). Although these disorders may represent clinically unusual distribution of the lesions, diagnosis and therapy are the same as for the more “typical” forms, and prognosis may be better than for those forms that also or only involve cornea.

C D

E

FIGURE 8-15. A, Complete resection of the third eyelid is required for larger tumors of the third eyelid. B, An eyelid speculum and mosquito hemostats are used to ensure adequate exposure of the third eyelid. Hemostats are then placed along the dorsomedial and ventrolateral borders of the third eyelid. C, Scissors are used to cut on the third eyelid side of each hemostat, and the anterior and posterior (bulbar) surfaces of sectioned conjunctiva are oversewn in a simple continuous pattern using 6/0 or 7/0 polyglactin 910 (Vicryl). D, The base of the third eyelid is clamped deep enough within the orbit that the gland and cartilage are completely resected, and the conjunctival edges are oversewn in the same manner as described in C. E, Final appearance showing the three lines of simple continuous suture, which ensure against orbital fat prolapse.

C D

FIGURE 8-16. Repair of a more major third eyelid laceration (minor lacerations do not need surgical correction). A, Torn third eyelid with a loose necrotic flap. B, Any loose or necrotic tissue should be resected. C, The bulbar and palpebral conjunctiva is mobilized from the underlying cartilage with tenotomy scissors. D, The mobilized conjunctiva is sutured with a continuous suture of 6/0 or 7/0 polyglactin 910 (Vicryl), with the knots tied on the anterior (palpebral) surface.

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