Audrey C. Hudson1 and Caleb Hudson2 1 Gulf Coast Veterinary Specialists, Houston, TX, USA 2 Nexus Veterinary Specialists, Victoria, TX, USA Prolapse of the gland of the nictitating membrane (NM), or “cherry eye,” is the most commonly diagnosed condition of the third eyelid (TEL).1 Nomenclature to describe this disorder varies among the literature, including “nictitating membrane gland prolapse,” “TEL gland prolapse,” and “cherry eye.” For the purposes of this chapter, we will use the term “TEL gland prolapse.” While the exact cause of TEL gland prolapse is unknown, laxity in the attachment of gland to the periorbita is thought to lead to the development of this condition.2 It is also theorized that young dogs exposed to new, environmental antigens can develop antigenic stimulation of the conjunctival lymphoid tissue, leading to TEL gland prolapse.3 Development of TEL gland prolapse typically occurs at an early age in dogs with 75% of cases diagnosed at less than a year of age.4 Presentation is commonly unilateral initially; however, contralateral gland prolapse can be present simultaneously or occur within months in many cases.4,5 Conversely, age and laterality of presentation are variable in cats.6,7 Commonly affected canine breeds include the American Cocker Spaniel, English Bulldog, French Bulldog, Lhasa Apso, Pekingese, Beagle, Shar Pei, Great Dane, and Cane Corso.4,5,8–10 Reported breeds of cats include the Burmese, Persian, and domestic short hair cat with the Burmese being overrepresented.7,11,12 A genetic basis has yet to be established.1,5 Seated in the ventromedial orbit, the TEL is a thin, reinforced membranous tissue that contributes to tear production, tear film distribution, and protection of the globe.1 Two connected pieces of cartilage forming a T‐shape within the TEL provide structural support to the membrane.13 The TEL cartilage is composed of hyaline cartilage in the dog but is primarily elastic in the cat.14 The thicker, vertically oriented cartilage forms the base and primary support of the TEL. It is oriented parallel to the direction of normal TEL excursions, which course ventromedially to dorsolaterally. The cartilage of the leading margin is thinner and positioned horizontally. Crescent‐shaped in the dog and reverse‐S in shape in the cat, the horizontal cartilage is connected perpendicularly to the vertical cartilaginous base.14 Both pieces of cartilage are concave, allowing for close apposition to the globe and smooth motion of the TEL over the corneal surface.13,14 Conjunctiva lining the globe courses anteriorly, forming a conjunctival sac, or bulbar conjunctival fornix, between the globe and TEL. This conjunctiva continues anteriorly lining both the posterior (bulbar) and anterior (palpebral) aspect of the TEL. The palpebral conjunctival fornix is formed by the junction of the palpebral conjunctiva of the TEL and the palpebral conjunctiva of the lower eyelid.14 While the overlying conjunctiva is loosely attached to the underlying structures of the TEL, the conjunctiva becomes firmly attached to the cartilage at the leading edge. The often‐pigmented leading edge of the TEL is the only visible portion of this structure in the awake dog and cat and can be seen adjacent to the ventromedial limbus.13,14 Surrounding the cartilaginous base of the TEL lies an accessory lacrimal gland that produces 30%–60% of the precorneal tear film.15 This gland produces seromucous secretions in the dog and serous secretions in the cat.13,14 The gland communicates with the bulbar conjunctival fornix via numerous small ductules, which transmit and release the glandular secretions into the fornix.13 A second accessory gland, the Harder’s gland or Harderian gland, can be present in addition to or in place of the TEL gland in many small mammals.14 Diseases and surgery of the Harderian gland are outside of the scope of this chapter. The bulbar conjunctiva of the TEL contains lymphoid tissue. Antigenic stimulation of the lymphoid tissue can cause hyperplastic changes resulting in a raised cobblestoned‐appearing swelling, which can be visible on external examination.13,16 Lymphoid hyperplasia can be differentiated from a prolapsed gland of the TEL, as the follicles are smaller, multifocal, and reside superficially within the bulbar conjunctiva of the TEL.13 A supportive ligament attached to the base of the TEL is formed by both the superficial and middle muscular fascia. Both of the fascial layers envelope the extraocular muscles and provide stabilization of the TEL as they attach to the orbital septum and limbus of the eye.13 Normally retracted in the ventromedial orbit, movement of the TEL is mainly passive secondary to globe positioning. TEL excursions are initiated upon blinking, contraction of the retractor bulbi muscle, and retraction of the globe causing TEL movement in a dorsolateral direction across the surface of the cornea.14 In the cat, the TEL has additional smooth muscle fiber attachments that are thought to cause active excursions of the TEL.1,14 The TEL remains retracted within the ventromedial orbit due to resting sympathetic innervation of periocular smooth muscles. Contraction of these smooth muscle fibers maintains the anterior positioning of the globe within the orbit along with retraction of the base of the TEL.13,14,17 Abnormal protrusion of the TEL can occur when resting enophthalmos is present, such as with the loss of sympathetic tone to the periocular structures, phthisis bulbi, or active contraction of the retractor bulbi muscle seen with ocular discomfort. Because of the finite orbital volume, orbital cellulitis secondary to periocular neoplasia, salivary gland disease, foreign bodies, and retrobulbar abscesses can cause abnormal protrusion of the globe along with protrusion of the TEL and its gland.1 Historically, prolapsed TEL glands were treated by surgical excision to resolve the unsightly appearance.18 In the 1980s, surgical gland repositioning was described and has become the recommended treatment for TEL gland prolapse. Surgical excision of the TEL gland significantly reduces precorneal tear film in both cats19 and dogs,20 in addition to degradation of the health of the corneal surface cells.21 Dogs with prolapsed TEL glands removed or left untreated have been shown to be more likely to develop keratoconjunctivitis sicca (KCS) months to years later.8,10 However, KCS can still occur after gland repositioning, especially in at‐risk dog breeds, including the American Cocker Spaniel, English Bulldog, and Lhasa Apso.8 Therefore, thorough client communication prior to surgery and continued monitoring of tear production postoperatively are important.8 Early in the disease process, massaging the displaced gland proximally into the ventromedial orbit can result in temporary repositioning. However, this technique only results in temporary correction, and long‐term success has not been reported.3 Topical anti‐inflammatories can serve as adjunctive therapy to help reduce secondary inflammation of the gland and conjunctiva that occurs with chronic gland prolapse. However, anti‐inflammatory therapy alone will not result in gland repositioning.3 Surgical repositioning techniques are the mainstay of therapy and include reinforcing the gland’s attachment to deeper structures or creating a pocket in which to bury the prolapsed gland.1,3 The attempt to find a cosmetically acceptable surgery with a low risk of TEL gland reprolapse has led to the development of a myriad of surgical techniques. An exhaustive review of all reported procedures is beyond the scope of this chapter. Some of the more notable reported procedures will be mentioned with further explanation of the common pocket and tacking techniques. Pre‐operative assessment of the TEL and prolapsed gland is necessary for accurate diagnosis and surgical planning. While the TEL gland is likely to be visible, the remainder of the TEL remains seated in the ventromedial orbit. Thorough assessment of the TEL and gland requires retropulsion of the globe and can be performed by applying gentle digital pressure to the globe. Digital pressure is applied over a closed upper eyelid, protecting the cornea from direct contact during this maneuver. The globe should retropulse easily and the TEL elevate passively. The gland will typically prolapse further, allowing a more thorough examination. Additional assessment of the TEL structures, including the leading edge and associated cartilage, the (vertical) cartilaginous base, and bulbar and palpebral conjunctival surfaces can also be performed. Globe resistance to retropulsion, TEL‐associated swelling not consistent with a soft, subconjunctival glandular structure, or inflammation not localized to the bulbar aspect of the TEL should be further evaluated for etiologies other than a prolapsed gland. After instillation of a topical anesthetic, such as proparacaine or tetracaine, a cotton‐tipped applicator or fine‐toothed forceps can be used for additional manipulation of the TEL and associated tissue.22 In middle‐aged and older patients that present with an acute TEL gland prolapse, careful assessment for other underlying causes of TEL gland protrusion is recommended.4 Given the delicate tissue and need for small movements with instrumentation, ophthalmic surgery is best performed sitting in a chair, with forearms resting on the surgical table and elbows bent at 90°.22 This positioning provides hand stabilization and improves fine motor control. In addition, specific ophthalmic instrumentation is recommended to prevent damage to the delicate, periocular structures and assure accurate technique. For all surgical procedures, the patient is placed in sternal recumbency with the head tilted 45°, rotating the surgical eye upward and positioning it near‐parallel with the surgical table. The fur is clipped in the periocular region, and the periocular region and conjunctival fornices are prepped with 5% betadine solution. Quarter‐draping with huck towels and towel clamps is performed to sterilely isolate the affected eye. Various anchoring procedures have been described in which the prolapsed gland is sutured to the episclera,23 sclera,24 extraocular muscle attachments,12,25 cartilage of the TEL,18 and ventral orbital periosteum.26–28 Many of the tacking procedures that require the gland to be sutured to the globe can be technically challenging, are associated with an increased rate of gland prolapse recurrence, and risk trauma to the eye. Therefore, tacking the gland to the orbital rim is one of the preferred anchoring techniques and will be described in more detail below (Surgical Techniques: Periosteal Anchoring Technique).3 Repositioning the gland within a conjunctival pocket has also been explored as an alternative to gland excision.8,29,30 Creation of a conjunctival pocket to contain the gland without residual postoperative protrusion proved to be challenging.8 A novel technique reported by Morgan et al.8 attempted to mitigate these complications while also improving postoperative cosmesis and maintaining normal TEL anatomy. The theoretical concern of TEL gland ductal occlusion associated with the use of a pocket technique has proved to be an uncommon occurrence.8,31 With an easy surgical learning curve and an excellent reported success rate, this procedure has become one of the most commonly utilized techniques for treating TEL gland prolapse in both the dog and cat and will be discussed in detail below (Surgical Techniques: Morgan Pocket Technique).1,8 Anchoring to the periosteum of the orbital rim can be performed through the periocular skin or through the conjunctiva. Because the periosteal tissue is quite tough and significant tissue purchase is needed for this technique to be successful, larger instrumentation is used. Fine‐toothed Bishop‐Harmon 0.8 mm 1 × 2 teeth forceps are used in place of Colibri 0.3 mm 1 × 2 teeth forceps. Derf needle holders are used in place of Castroviejo needle holders. In contrast to the pocket technique, nonabsorbable sutures, such as nylon or polypropylene, are used to anchor the gland. A larger, 13 mm or longer, 3/8 circle needle can be used to accommodate the longer suture bites needed to pass between the periosteum and the gland. Figure 3.1 Instrumentation commonly utilized during TEL gland repositioning surgery. (a) Ophthalmic forceps, including Bishop‐Harmon 0.8 mm, 1 × 2 teeth thumb forceps (top) and Colibri 0.3 mm, 1 × 2 teeth forceps (bottom). (b) Ophthalmic blades including #15 Blade on a Bard‐Parker handle (top) and 6400 Beaver blade with handle (bottom). (c) Ophthalmic scissors including Steven’s tenotomy scissors (top) and Westcott tenotomy scissors (bottom). (d) Ophthalmic needle holders, including Derf needle holders (top) and Castroviejo needle holders (bottom). Source: © Audrey Hudson. Position and sterilely prepare the patient as described above. After palpating the inferior orbital rim, use a #15 scalpel blade on a Bard‐Parker handle to make a skin incision along the ventral, bony orbit. The initial incision is parallel to and 2–3 cm inferior to the lower eyelid margin (Figure 3.2). Bluntly dissect the subcutaneous tissue to expose the periosteum with Steven’s tenotomy scissors. The periosteum can be identified by a lighter pink‐to‐white color, distinct from the glossier surrounding subcutaneous tissue (Figure 3.3). Take a suture bite through the periosteum using 4‐0 nonabsorbable suture (Figure 3.4
3
Surgery for the Prolapsed Third Eyelid Gland
Introduction
Indications/Pre‐operative Considerations
Medical Management
Surgical Management
Pre‐operative Considerations: Diagnosis
Pre‐operative Considerations: Instrumentation
Recommended Surgical Instrumentation
Surgical Techniques
Periosteal Anchoring Technique
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