Ocular Manifestations of Systemic Diseases in Small Animals

by: Dennis E. Brooks, DVM, PhD, Diplomate ACVO

Current Concepts in Veterinary Ophthalmology
~ November 1, 2003 ~

Anchor Jump Menu:
Introduction Bacteria Infections Distemper Hepatitis Feline Herpes
Feline Peritnitis Feline Leukemia Toxoplasmosis Fungal Disease Ehrlichia
Chlamydia Psittaci Systemic Disease Hyperviscosity Hypertension Horner's Syndrome
Uveodematological Reticulosis Lymphosarcoma Diabetes Mellitus Masticatory Myositis
Extraocular Myositis Entropion Eyelid Neoplasms Eyelash Disease KCS
Lacrimal System Punctal Membranes Conjunctiva    


Ophthalmic examination of animals with systemic disease is an important diagnostic method of categorizing and differentiating systemic disease processes. Infectious, neoplastic, autoimmune, nutritional, toxic and metabolic diseases may all have early and prominent ocular manifestations. Visual status may also be important to owners attempting to decide how aggressively they wish to pursue diagnostic and therapeutic options in the treatment of systemic diseases.

Back to top



Bacteremia due to Staphylococcus sp, Streptococcus sp, E. coli, and other bacteria can cause anterior or posterior uveitis, endophthalmitis, chorioretinitis, and optic neuritis. The ocular disease occurs from embolization in pyometra, prostatitis, pancreatitis, bacterial endocarditis, periodontal disease, and salmonellosis, or as an immune-mediated phenomena associated with circulating antigen-antibody complexes (chronic inflammatory disease processes). Leptospirosis in dogs may have conjunctival hemorrhages, icterus, and hyphema and signs of anterior uveitis due to an immunologic reaction, and/or direct infection of the uvea. Leptospirosis has mild or inapparent ophthalmic signs in cats. Brucella canis in dogs has ophthalmic signs of recurrent corneal edema, anterior uveitis, chorioretinitis, optic neuritis, endophthalmitis, and secondary glaucoma. Aqueous paracentesis reveals increased proteins, erythrocytes, neutrophils, and mononuclear leucocytes. The organism can be cultured from aqueous and vitreous, and titers detected in serum and aqueous humor. Borreliosis (Lyme disease) caused by spirochete Borrelia burgdorferi is transmitted by the tick Ixodes dammini. It is associated with anterior uveitis in dogs. Clostridium tetani releases a potent neurotoxin which is associated with nictitans protrusion, except in exophthalmic breeds. Mycobacterium bovis is rare today, although cats may acquire it from the milk of infected cows. Ocular features include conjunctivitis, keratitis, granulomatous uveitis, and chorioretinitis.

Back to top




 Figure 13: Dog showing keratoconjunctivitis sicca (KCS)


Canine Distemper Virus has systemic features ranging from a mild cough to severe coughing, dyspnea, lethargy, anorexia, vomiting, diarrhea, and CNS signs. Ocular signs include serous to mucopurulent bilateral ocular discharge, optic neuritis (sudden blindness), chorioretinitis, retinal detachment, keratoconjunctivitis sicca (KCS) (Figure 13) that may last 4-8 weeks or be permanent, corneal ulcers, and cortical blindness. Chronic retinochoroidopathies present as areas of increased tapetal reflectivity (gold-medallion lesions) and altered pigmentation in tapetal and non-tapetal areas.

Conjunctival scrapings reveal mononuclear leucocytes and giant cells initially, then neutrophils. Intracellular inclusion bodies in conjunctival epithelial cells may be noted. Treatment is aimed at controlling secondary infections. Supportive treatment improves the chance for recovery and quality of life.

Back to top



Ocular complications include bullous keratopathy, keratoconus/keratoglobus, phthisis bulbi, and secondary glaucoma. Complications are most likely to occur in the Afghan. Canine Herpes Virus may have a transient conjunctivitis, panuveitis, keratitis, cataracts, and optic neuritis and atrophy. Retinal dysplasia may be found in neonates.

Diagnosis is based on the clinical history and signs, and demonstration of increasing antibody titer in paired serum samples. Therapy includes topical corticosteroids, atropine, and nonsteroidal antiinflammatories.

Back to top



Early signs of herpesvirus conjunctivitis include a bilateral serous ocular discharge that becomes mucopurulent with time. Secondary bacterial infections enhance the mucopurulent exudate. Conjunctivitis is found in many types of eye diseases. It may be infectious (herpes, calici, mycoplasma and chlamydia in cats) or noninfectious. It may be primary, or be secondary to ulcerative keratitis, episcleritis, glaucoma, anterior uveitis, eyelid disease (entropion, ectropion, ectopic cilia, blepharitis), orbital cellulitis, nasolacrimal duct obstruction, keratoconjunctivitis sicca, atopy, environmental irritation, and neoplasia (lymphoma). Therapy of herpesvirus conjunctivitis consists of topical antiviral preparations and broad spectrum antibiotics to control the secondary bacterial infection. The efficacy of the antiviral medication in controlling the herpesvirus conjunctivitis (without corneal involvement) is variable. Herpes virus vaccines are available for cats; however, herpes virus conjunctivitis occurs in vaccinated cats.

Recurrent herpes virus may be associated with the immunosuppression by FIV/FeLV. Initial treatment includes trifluorothymidine (1%) applied to the affected eye (s) 5 times a day. Acyclovir is useful at 200 mg orally TID in combination with interferon. Systemic interferon may be beneficial in cats that are refractory to other therapies. Alpha 2 interferon may be administered 3 U/ ml / cat orally q24h for the life of the cat, or 30 U/ml q24h orally for 7 days, off 7 days, on 7 days, etc. Oral Lysine (400 mg per os per day) can reduce viral shedding in latently infected cats. Lodoxamide 0.1% (Alomide) TID is a mast cell stabilizer for feline herpes/eosinophilic keratitis.

Client education is important. Herpes virus infection may be chronic and recurrent especially during times of stress. Recurrent and chronic herpes infections may suggest systemic immunosuppression so cats should be evaluated for FeLV and FIV.

Back to top



causes uveitis and chorioretinitis

Back to top



causes uveitis and chorioretinitis

Back to top



The uveitis is frequently documented as multiple foci of retinitis or retinochoroiditis,(Fig 10) with varying degrees of anterior uveitis, in cats. In dogs, chorioretinitis, optic neuritis, and less frequently, anterior uveitis and inflammation of extraocular muscles are present. Owners should be instructed in the basic hygienic rules to prevent toxoplasmosis. Treatment for toxoplasmosis includes antimicrobial agents (sulfadiazine, pyrimethamine, clindamycin) and supportive therapy. In case of localized ocular involvement, the standard treatment for uveitis is indicated.

Back to top



Systemic mycotic infections which commonly involve the eyes include cryptococcosis, histoplasmosis, blastomycosis, and coccidioidomycosis. Inhalation is believed to be the primary route of infection with hematogenous spread to the eye. Diagnosis is based on clinical and ocular signs, radiographs, stained smears from tissue samples, ocular paracentesis, peripheral lymph node aspirates, and serology. Miscellaneous fungi/yeasts causing conjunctivitis, keratitis, and/or chorioretinitis include Nocardiosis, Candidiasis, Geotrichosis, Aspergillosis, and Paecilomycosis. The systemic aspergillosis of German Shepherds often has ocular manifestations.

Back to top



Systemic features include lymphadenopathy, fever, nasal discharge, thrombocytopenia, and pancytopenia, with an underlying vasculitis. The ophthalmic signs include tortuous retinal vessels with gray perivascular circular retinal foci in the early stages. Chorioretinitis and retinal vasculitis appearing as dark grey spots with surrounding hyperreflectivity in the tapetal fundus, subretinal hemorrhages, retinal detachment, optic neuritis, and papilledema are found in the later stages. Anterior uveitis, iridal petechiae, hyphema, and keratic precipitates may also be prominent. In the clinical setting, a diagnosis of ehrlichiosis is usually made on the basis of clinical signs, hematologic abnormalities and serology. Nonregenerative anemia and thrombocytopenia are the predominant hematologic findings. See Chapter on infectious diseases. Tetracyclines are used for systemic therapy. Anterior uveitis is treated with topical corticosteroids and atropine.

Back to top



Initially, the disease is unilateral, becoming bilateral in 7 to 14 days. Early in the disease, the conjunctiva is chemotic, glistening, and grayish-pink, and the ocular discharge is serous. Sneezing is present early in the disease. Severe blepharospasm occurs and may cause a secondary spastic entropion. Conjunctivitis is found in many types of eye diseases. It may be infectious (herpes, calici, mycoplasma and chlamydia in cats) or noninfectious. It may be primary, or be secondary to ulcerative keratitis, episcleritis, glaucoma, anterior uveitis, eyelid disease (entropion, ectropion, ectopic cilia, blepharitis), orbital cellulitis, nasolacrimal duct obstruction, keratoconjunctivitis sicca, atopy, environmental irritation, and neoplasia (lymphoma). Treatment of chlamydial conjunctivitis consists of tetracycline ophthalmic ointment three times daily for 4 weeks. Vigorous therapy should be continued for 1 to 3 weeks after clinical signs subside. Follicular conjunctivitis is treated by anesthetizing the cat and rupturing the follicles by vigorously rubbing with a gauze sponge or scraping with a surgical blade. Topical tetracycline and corticosteroids are then applied, unless the corneal epithelium is damaged. Recurrence of disease is common in catteries and research colonies due to short immunity of Chlamydia psittaci. Chlamydia psittaci may cause disease in man; therefore, owners and technicians are advised to exercise care and observe strict hygiene when handling or treating infected cats.

Back to top



Ocular manifestations of hypercalcemia from hyperparathyroidism, neoplasia, renal failure, and hypoadrenocorticism may be associated with white, perilimbal calcium crystals on the conjunctiva, corneal degeneration, and cataracts. Sustained hypocalcemia due to primary hypoparathyroidism, chronic renal failure, and intestinal malabsorption can cause cataract formation.

Back to top



This hyperviscosity results in thromboembolism, hemorrhage, and CNS and ocular disturbances. Ocular changes are noticed very early in disease and include retinal hemorrhage, retinal venous dilatation and segmentation, retinal vascular tortuosity, microaneurysms of the retina, subretinal hemorrhage, retinal detachment,(Fig 20) perivascular retinal folding, and papilledema. Anterior uveitis and secondary glaucoma may also be present. A coagulation assessment (platelet count, partical thromboplastin time, prothrombin time), serum protein electrophoresis, and serum viscosity measurements should be undertaken. Animals should have a thorough funduscopic examination. Plamapheresis may be used to treat the hyperviscosity. Specific antineoplastic therapy directed at the underlying disease is indicated.

Back to top



Ocular features include retinal arteriolar tortuosity, pre-retinal hemorrhage, retinal edema, perivasculitis, anterior uveitis, vitreal and anterior chamber hemorrhage, retinal detachments, and retinal atrophy.. In severe cases, irreversible blindness occurs. The diagnosis is based on serial measurements of blood pressure. Complete blood counts, urinalysis and serum biochemical profiles should be undertaken in all patients. Treatments include salt restricting diets, diuretics, and calcium channel blockers such as amlodipine (0.625 mg/5 kg body weight, q24h).

Back to top



The Horner's miotic pupil is not pin-point in room light, constriction still occurs and dilation in dark light occurs, but not as much dilation as a normal pupil (no dilation beyond the size of the pupil with a resting iris sphincter muscle). The causative lesion can occur anywhere along the sympathetic chain. Uveitis has nictitans prominence and a miotic pupil with aqueous flare, conjunctivitis and blepharospasm. The diagnosis is based on a complete physical examination and neurologic, otoscopic and ophthalmologic examinations. The disorder spontaneously resolves in some patients.

Back to top



Severe, bilateral panuveitis and hypotony, with secondary cataracts, glaucoma, retinal detachments, and blindness are common. Iris and retinal depigmentation, and poliosis/vitiligo of the face and muzzle are noticed. Special stains should be requested in the presence of granulomatous infiltrates in an attempt to identify microorganisms. Short term success with systemically administered corticosteroids or azathioprine is good, but recurrence is common. Topical treatment of the uveitis is required.

Back to top



Ocular features include acute, bilateral blindness with widely dilated, nonresponsive pupils. Uveitis, optic neuritis (hyperemic, swollen, elevated optic disc, disc hemorrhage, peripapillary engorged vessels), retinal inflammation (white perivascular cuffs and yellow-white patches), retinal detachment, and secondary glaucoma are common. The eye may appear normal if the optic nerve involvement is posterior to the globe. The diagnosis can only be confirmed at necropsy or by brain biopsy. Analysis of CSF (increased CSF protein and pleocytosis) may enable a reliable tentative diagnosis to be made. Gradual improvement with corticosteroid treatment is possible, but the response is transient.

Back to top



Lymphosarcoma in dogs and cats may manifest as corneal edema, centrally migrating white bands of neoplastic cells, stromal hemorrhage, corneal vascularization, anterior uveitis with hyphema, hypopyon, keratic precipitates and secondary glaucoma, and tortuous retinal vessels, retinal hemorrhages, perivascular sheathing, retinal detachment, or retinal tissue infiltration by tumor cells. Conjunctivitis, hyphema, anterior uveitis, retinal detachment and glaucoma may be caused by lymphosarcoma. Lymphadenopathy combined with bilateral anterior uveitis or intraocular hemorrhages should cause suspicion of lymphoma. Enlarged lymph nodes should be investigated by fine needle aspiration.

Anterior uveitis and hyphema should be treated by topical corticosteroids and atropine. Medical protocols for treatment of lymphosarcoma should be instituted.

Back to top



There is a high incidence of cataracts in diabetic dogs, with many cataracts apparently developing rapidly over days to weeks. Most diabetic dogs form cataracts within 2.5 years after diagnosis. Early cataractous changes appear as vacuoles (Fig 37) in the subepithelial equatorial cortex which progress to mature, intumescent cataractous lenses with prominent Y-suture clefting. Cataracts occur much less frequently in diabetic cats as the diabetic cat lens contains less aldose reductase activity. Anterior uveitis is also found in some canine diabetics. Diabetic retinopathy is slow to develop in diabetic dogs and cats. Treatment can be divided into the acute management of diabetic ketoacidosis and the stabilisation of the uncomplicated diabetic. The ketoacidotic dog can be stabilised as for the uncomplicated case, once it has started to feed normally. Surgery is necessary to treat the cataracts.

Back to top



Masticatory muscle myositis of the masseter, pterygoid, and temporalis muscles may develop acute, painful exophthalmos, or chronic muscle atrophy with enophthalmos and nictitans protrusion. Most dogs are presented with anorexia and depression, although tonsillitis, submandibular and prescapular lymphadenopathy and pyrexia may occur.

Differential Diagnosis: Orbital cellulitis and orbital neoplasia. The diagnosis is based on electromyelography which reveals abnormal spontaneous activity, peripheral eosinophilia, elevated serum creatine phosphokinase, temporalis muscle biopsy, and the demonstration of serum 2M autoantibodies. Systemically administered corticosteroids are indicated in acute disorders. Uncontrolled myositis leads to muscle atrophy.

Back to top



Extrocular muscle myositis is common in 8-10 month old Golden Retrievers. The specific cause is unknown at present.

Extraocular muscle myositis is an immune mediated disease directed against the Type I myofibers of the extraocular muscles. The clinical signs are bilateral in most cases, generally non-painful, chemosis precedes exophthalmos in 81% of cases, and optic nerve impingement with optic neuritis may occur to cause blindness. Differential Diagnosis: Orbital cellulitis and orbital neoplasia. Diagnosis is by serum and muscle biopsy for detection of Type I myofiber antibodies.

Treatment is the same as for masticatory muscle myositis.

Back to top



Entropion is an inward rolling of the eyelid margin. This causes the eyelid hairs to rub on the cornea. It is most common in dogs and sheep, and uncommon in horses and cats (except for Persians).

Entropion can be either congenital or acquired. Congenital entropion may not manifest itself initially, and it may be inherited in certain breeds. Commonly affected breeds include Chow, English Bulldog, Toy and Miniature Poodle, Norwegian Elkhound, Great Dane, Rottweiler, Pug, Shar Pei, and sporting breeds. It is sometimes seen in combination with ectropion. Acquired entropion can be spastic (secondary to chronic irritation and pain) where spasms of the orbicularis oculi muscle occur. Given enough time, it may be irreversible. If spastic entropion is suspected, a drop of topical anesthetic should be placed on the cornea to relieve superficial pain and the eye should be observed shortly after topical anesthesia for resolution of the entropion. Acquired entropion can also be cicatricial, and results from prior or previous eyelid damage.

Clinical signs seen with entropion include epiphora, blepharospasm, conjunctivitis, and keratitis. The amount and type of signs varies with the extent of involvement and duration. Medial entropion may occlude the lower lacrimal punctum.

Surgical techniques should always under-correct slightly for optimal results. Post-operative scarring adds to the extent of the correction. DO NOT SURGICALLY CORRECT AN IMMATURE ANIMAL (< 6 MO), IF POSSIBLE. Manage medically or with temporary sutures as they may improve spontaneously or become more severe with further growth.

Medical treatment of entropion involves ocular lubricant ointments, such as Lacrilube, Dura Tears, or Hypotears. This is sometimes used to protect the cornea from the eyelid hairs while waiting for an animal to mature.

Surgical treatment can be either temporary or permanent. Temporary procedures involve using nonabsorbable sutures to evert or "tuck" eyelids in immature animals (usually less than 6 months of age). Sutures are left in place 10 to 14 days, and can provide dramatic results in Shar Pei puppies. Staples and superglue have also been utilized. Permanent procedures are more invasive. The AKC (12/93) says that dogs having entropion surgery may not be shown.

Back to top



The majority of canine eyelid tumors are benign. Those that appear histologically malignant tend to be infiltrative but rarely metastasize.

  1. Sebaceous gland adenoma - Most common lid tumor in dogs, frequently found in older dogs. Visible through the conjunctival surface and extend onto the eyelid. Should be removed.
  2. Melanomas - Frequently darkly pigmented, but not always. Tend to occur at eyelid margin. Early surgical resection is recommended. May recur. Not very responsive to other types of therapy.
  3. Squamous cell carcinoma - Rare in the dog. Most common lid tumor of cats, cows and horses. May be rapidly growing, highly invasive. Tend to ulcerate early and will occasionally metastasize. Early biopsy and wide surgical excision are imperative. Radiation therapy decreases the chance of recurrence.

Back to top




The most common form of eyelash disease in dogs. Cilia arising from meibomian glands and exit from the normal meibomian gland opening at the lid margin (single cilia - distichiasis; multiple cilia - districhiasis). May occur on both upper and lower eyelid. Clinical signs include epiphora, blepharospasm, and conjunctivitis, and sometimes keratitis. Only those hairs creating a problem need to be treated.

Treatment can be medical (if only a few distichia present and problem is minor, or if animal is poor surgical candidate - use sterile lubricants as needed) or surgical. Epilation is pulling out the hair with topical anesthesia and cilia forceps. This provides temporary relief, but hairs do grow back. Electrolysis involves running a fine needle along hair shaft to the root and using heat to destroy the follicle. Cryosurgery works well but depigments lid margins. The depigmentation is usually transient, but can be permanent.

Ectopic Cilia

Cilia grows from the meibomian gland but exits through the palpebral conjunctiva. Occurs primarily in upper eyelid, frequently near the center. Often very small and magnification is required to observed these. Fluorescein stain may coat the mucous and tears on the cilia making it easier to visualize. Animals with ectopic cilia often have ocular (corneal) pain and chronic corneal erosions. Diagnosis is made with the eyelid everted and magnification to look for a papilla of tissue containing the hair(s). Conjunctival resection is the preferred treatment. Recurrence frequent after electro-epilation.

Nasolacrimal System

The nasolacrimal system is comprised of secretory and drainage apparatuses. Tears are secretions from several glands, and the glands involved are varied by species. Aqueous tear secretions come from the main lacrimal glands (orbital lacrimal gland and gland of the third eyelid in domestic animals.

Tear drainage is accomplished via nasolacrimal puncta and ducts. The duct enters the nasal cartilage and emerges in the nasal cavity. In some brachycephalic dogs and in most cats, the nasolacrimal duct terminates in the mouth.

Back to top



Aqueous deficiency of the precorneal tear film (PTF) causing progressive inflammatory changes of the cornea and conjunctiva.


  1. Clinical signs
  2. Schirmer tear test: Normal 15-25 mm/minute; Suspicious = 8-10 mm/minute; Low = <8 mm/minute
  3. Rose bengal stain - epithelium of conjunctiva and cornea will remain red if devitalized or necrotic.
  4. The mean PRT absorbence value in cats (23.0 mm/15 seconds) is approximately two-thirds the mean PRT absorbence value in dogs (34.2 ± 4.4 mm/15 seconds).



Breeds at Risk - English Bulldog , West Highland White Terrier, Lhasa Apso, Pug, Cocker Spaniel, Pekingese, Yorkshire Terrier, Shih Tzu, Miniature Schnauzer, Boston Terrier



  1. Congenital/inherited: Pug, Yorkshire Terrier, Miniature Schnauzer, American Cocker Spaniel, English Bulldog, Beagle
  2. Drug related:
    - Atropine: Topical and systemic
    - Sulfonamides: sulfadiazine, salicylazosulfapyridine (Azulfidine®), Tribrissin®- small dogs at increased risk
  3. Systemic diseases: Canine distemper virus
  4. Chronic blepharoconjunctivitis - scarring of lacrimal ducts
  5. Neurogenic
  6. Other "associated" diseases: **Immune related disorder suspected in up to 40% of cases. Hypothyroidism, Hyperadrenocorticism, Diabetes mellitus, Demodectic mange, SLE, RA
  7. Trauma to the orbit and lacrimal gland
  8. Iatrogenic - removal of the superficial gland of the nictitating membrane

Back to top


Clinical Signs

blepharospasm, conjunctivitis, mucoid discharge, corneal ulcers, dry appearance, owners frequently complain of "chronic eye infection", copious, mucoid-mucopurulent discharge, dull cornea with neovascularization, pigmentation of cornea, improvement with any topical medication.



Always attempt 1-2 months of medical treatment because the problem may be transient. Owner compliance may be difficult. Goals are to remove pain and maintain vision:

  1. Replace tears - Hypotears (CIBA Vision); Tears Naturale (Alcon); Lacrilube (Allergen); Duratears (Alcon); Lacriserts (Merck)
  2. Stimulate production of tears
    Topical 0.2% Cyclosporine (OPTIMUNE): DRUG OF CHOICE FOR KCS, BID
    Topical 0.03% Tacrolimus BID for CSA nonresponders.
  3. Control bacterial flora - topical broad spectrum antibiotic BID, eg. triple antibiotic or chloramphenicol ointment
  4. Control inflammation - topical corticosteroids, may combine with topical antibiotic (TriOptic-S, triple antibiotic with hydrocortisone); USE ONLY IF NO CORNEAL ULCERATION!!

Surgical therapy

  1. Conjunctival flap - Deep corneal ulcers, to provide corrective tissue and blood vessels.
  2. Parotid duct transposition
    - patients who do not respond to medical therapy over 6-12 week period of time
    - patients whose owners cannot manage medical therapy
    - remember, saliva is not a perfect substitute but is adequate in most cases.

Back to top



Outflow System: Most common clinical sign is epiphora.

Back to top



American Cocker Spaniel, Toy and Miniature Poodle
Obstructions of Nasolacrimal System


  1. Congenital absence of inferior canaliculus
  2. Inflammatory = dacryocystitis
  3. Foreign body
  4. Secondary to scarring - traumatic, inflammatory

Signs - Depends on cause:

  1. Inflammatory/foreign body/neoplastic
    - epiphora - mucopurulent discharge
    - conjunctivitis
    - pain on palpation of medial canthus region
    - abscessation in severe cases
  2. Congenital/scarring/neoplastic
    - epiphora


  1. Negative fluorescein passage
  2. Flushing duct to recover material
  3. Dacryocystorhinography


  1. Infectiona and Anti-Inflammatory
  2. Systemic antibiotics and corticosteroids

Back to top






Most common extraocular problem in practice

Diagnostic tests for conjunctivitis

  1. STT and PRT- routine on all conjunctivitis cases
  2. Culture/sensitivity - fornix, not routinely done
  3. Cytology - topical anesthetic, spatula
  4. IFA and PCR tests for herpes and chlamydia in cats


Etiologies of conjunctivitis

  1. Bacterial conjunctivitis = purulent discharge
  2. Viral conjunctivitis - frequently bilateral, may be unilateral
  3. Allergic conjunctivitis - frequent cause
  4. Physical irritation conjunctivitis - wind, dust, foreign bodies, eyelid disease, etc.; frequent cause
  5. Keratoconjunctivitis sicca conjunctivitis


Nictitating Membrane - Eversion of Cartilage

  1. Cartilage is abnormally formed, causes nictitans to roll inward or outward. Seen in Basset Hounds and Weimaraners.
  2. Decreased function, cosmetically unacceptable. Can lead to chronic irritation. Can be associated with "cherry eyes".
  3. Treatment = surgical removal of affected cartilage


Hypertrophy and prolapse of nictitans gland (CHERRY EYE)

  1. Primarily seen in young dogs, less than 2 years
  2. Most common in Beagles, American Cocker Spaniels, Pekingese
  3. Gland protrudes above free border of the TE, becomes inflamed and enlarged. May see epiphora, mucoid discharge and conjunctival inflammation.
  4. Treatment
    1. Medical - physically replace gland, topical corticosteroids - frequently recurs.
    2. Surgical: Repositioning of gland to normal location. Gland can be "tacked" into normal position by placing a suture into gland and anchoring it to the periosteum of the inferior orbit, the ventral oblique muscle, or can be buried in a pocket of conjunctiva. Excision of the gland - the nictitans itself should not be removed in all cases. May predispose to keratoconjunctivitis sicca (KCS).

Back to top


Dennis E. Brooks, DVM, PhD, Diplomate, American College of Veterinary Ophthalmologists is a professor of ophthalmology at the College of Veterinary Medicine, University of Florida.

Reproduced with permission.