Canine Cherry Eye Study Guide

Overview and Clinical Importance

Cherry eye is the common term for prolapse of the gland of the third eyelid (nictitating membrane), clinically known as prolapsed nictitating membrane gland (PNMG). This is the most common disorder affecting the canine third eyelid and represents a significant ophthalmic condition encountered in veterinary practice.

The condition occurs when the nictitating membrane gland, which is normally anchored to the base of the third eyelid by connective tissue attachments to the periorbita, prolapses dorsally and becomes visible as a smooth, pink to red, round mass protruding from behind the leading edge of the third eyelid. The appearance resembles a cherry, hence the common name.

Understanding cherry eye is critical for NAVLE success because it requires knowledge of ocular anatomy, appropriate surgical management principles, and recognition that gland removal is contraindicated due to the risk of subsequent keratoconjunctivitis sicca (KCS/dry eye).

Anatomy of the Third Eyelid

The third eyelid (nictitating membrane or nictitans) is a crescent-shaped conjunctival fold located in the ventromedial aspect of the eye, conforming to the shape of the cornea. It provides essential protection and lubrication to the ocular surface.

Key Anatomical Components

• T-shaped cartilage: Provides structural support; the horizontal portion lies along the leading edge while the vertical shaft extends into the base
• Nictitating membrane gland (third eyelid gland): Serous-mucous gland located at the base of the third eyelid, surrounding the vertical portion of the cartilage
• Conjunctival covering: Thin mucous membrane covering both surfaces
• Connective tissue attachments: Anchor the gland to the periorbital tissues

Tear Production Contribution

The nictitating membrane gland is one of two lacrimal glands responsible for the aqueous portion of the tear film. The third eyelid gland produces approximately 30-50% of the total aqueous tear production (with some sources citing up to 60%), with the remainder produced by the orbital lacrimal gland located dorsal to the globe.

Etiology and Pathophysiology

The precise pathogenesis of cherry eye remains incompletely understood. The condition is believed to result from weakness or defect in the connective tissue (retinaculum) that anchors the gland to the periorbital tissues, allowing the gland to prolapse dorsally above the leading edge of the third eyelid.

Contributing Factors

• Genetic predisposition: Strong breed associations suggest hereditary weakness in connective tissue attachments; FGF4L1 retrogene insertion has been associated with cherry eye in genome-wide studies
• Brachycephalic conformation: Shallow orbits and altered orbital anatomy in flat-faced breeds; brachycephalic dogs have 6.9 times the risk compared to mesocephalic breeds
• Lymphoid hyperplasia: Inflammation and enlargement of lymphoid tissue within the gland may contribute, particularly in young dogs exposed to environmental allergens
• Young age: Most cases occur in dogs less than 2 years of age, suggesting developmental weakness; dogs under 1 year have 10.8 times the odds compared to dogs 2-4 years

Breed Predispositions

Research from VetCompass and other epidemiological studies has identified significant breed-specific risk factors:

"CHERRY BULLDOGS" C - Cocker Spaniel (American and English) H - Hounds (Beagle, Bloodhound, Basset) E - English Bulldog R - Rottweiler R - Really big dogs (Mastiffs, Great Dane, Saint Bernard) Y - Young dogs (less than 2 years)

Clinical Presentation

Signalment

• Age: Most commonly affects dogs less than 2 years of age; median age at diagnosis is approximately 7.5 months (0.63 years)
• Breed: Strongly overrepresented in predisposed breeds; purebred dogs at higher risk than mixed breeds
• Sex: No significant sex predisposition; both males and females equally affected

Clinical Signs

Diagnosis

Diagnosis of cherry eye is primarily clinical, based on the characteristic appearance of a pink to red, smooth mass protruding from the medial canthus in a young dog of a predisposed breed.

Diagnostic Approach

• Complete ophthalmic examination: Assess both eyes; check for bilateral involvement
• Schirmer tear test (STT): Measure baseline tear production (normal greater than 15 mm/min in dogs); important for comparison post-operatively
• Fluorescein staining: Rule out corneal ulceration secondary to exposure or self-trauma
• Tonometry: Intraocular pressure measurement to rule out concurrent glaucoma
• Third eyelid evaluation: Check for scrolled/everted cartilage which may occur concurrently, especially in giant breeds

Differential Diagnoses

Treatment

Surgical replacement (repositioning) of the prolapsed gland is the gold standard treatment. Medical management alone is generally ineffective for permanent resolution, and surgical excision of the gland is strongly contraindicated.

Surgical Techniques

Several surgical techniques have been described, broadly categorized into pocket (envelope) techniques and anchoring techniques:

Perioperative Management

Complications and Prognosis

Potential Complications

• Re-prolapse (recurrence): Most common complication; occurs in 5-20% of cases; higher risk in English Bulldogs and Neapolitan Mastiffs; may require repeat surgery with alternative or combined technique
• Keratoconjunctivitis sicca (KCS/dry eye): May develop if gland function is compromised; approximately 20% of dogs develop tear production problems after surgery; requires lifelong monitoring with annual STT
• Cyst formation: May occur if pocket technique completely encloses the gland without drainage openings
• Corneal ulceration: May occur from suture abrasion if knots contact cornea; reason to place knots on anterior (palpebral) surface
• Contralateral prolapse: Many dogs will develop cherry eye in the opposite eye; some surgeons advocate prophylactic treatment

Prognosis

The prognosis for cherry eye is generally excellent with appropriate surgical management. Key prognostic factors include:

• Earlier surgical intervention associated with better outcomes
• Chronic prolapse with significant gland inflammation may have higher recurrence rates
• Certain breeds (English Bulldog, Neapolitan Mastiff) have higher recurrence rates
• Combined techniques may be needed for recurrent cases

Consequences of Gland Excision (Why NOT to Remove)

Historical treatment involved excision of the prolapsed gland, but this approach has been shown to have serious long-term consequences:

• 29-57% reduction in Schirmer tear test values following gland removal
• 42.8-68% of dogs with excised glands develop KCS
• KCS requires lifelong topical medication (cyclosporine or tacrolimus) multiple times daily
• Only 10.5% of dogs with surgically replaced glands develop KCS
• Excision only indicated in rare cases: irreparable trauma, confirmed neoplasia, or severely fibrosed non-functional gland

Exam Focus: NAVLE commonly tests the knowledge that gland excision leads to KCS. Remember: excision results in 42-68% KCS rate vs only 10% with replacement. Excision = dry eye = lifelong topical medications = contraindicated!

Associated Condition: Keratoconjunctivitis Sicca (KCS)

Understanding KCS is essential when managing cherry eye, as it is the primary reason gland preservation is critical. Keratoconjunctivitis sicca is chronic inflammation of the cornea and conjunctiva resulting from deficiency in the aqueous portion of the tear film.

Clinical Signs of KCS

• Thick, ropey, mucoid to mucopurulent discharge
• Conjunctival hyperemia
• Corneal vascularization, pigmentation, and scarring
• Corneal ulceration (in chronic cases)
• Blepharospasm and ocular pain

KCS Management

• Cyclosporine (Optimmune) 0.2%: Immunomodulator; suppresses immune-mediated gland destruction; mainstay of therapy; applied 1-2 times daily
• Tacrolimus 0.02-0.03%: Alternative immunomodulator for cyclosporine non-responders
• Artificial tears: Lubricants to supplement tear film; used frequently
• Parotid duct transposition: Surgical option for refractory cases; redirects saliva to lubricate the eye