Progressive Retinal Atrophy (PRA)

by: By Karyn Colman, B.Vet.Med., MRCVS

According to Gelatt's Veterinary Ophthalmology (1999), PRA is a term for a group of hereditary diseases that are characterized by a degeneration or dysplasia (abnormal development) of the photoreceptors at the back of the eye. The changes are progressive and result in a loss of vision. All forms of PRA can be detected by trained Veterinary Ophthalmologists examining the back of the eye (once the visible changes are present), and incidences of PRA are included in the CERF statistics. A dog with PRA will not receive CERF certification. Electroretinograms (ERG) can detect changes in the function of the retina earlier than CERF examination can detect visible changes to the eye.

There are two main classifications of the disease processes involved in PRA:

  1. a primary effect on the photoreceptors (generalized PRA),

  2. abnormalities of the pigment epithelium behind the photoreceptors which causes secondary photoreceptor degeneration (central PRA or, more recently, RPED).


Central PRA is much less widespread in pure-bred dogs, apparently affecting Retrievers (Labrador and Golden) and Collie breeds almost exclusively. The progression of the disease is slower than GPRA and the dog may not become totally blind. This form of PRA has not, to date, been recorded in Alaskan Malamutes.

Generalized PRA is more widespread among the breeds and is a form of PRA that has been documented to affect the Alaskan Malamute in North America and in Europe. In generalized PRA the disease process usually leads to complete blindness. Generalized PRA is currently divided into two types of diseases:

  1. Early onset (retinal dysplasias),

  2. Later onset (prcd - progressive rod-cone degeneration).


The early onset retinal dysplasias result from abnormal development of the photoreceptors and breeds so affected can start to show signs as early as 12 weeks of age. For later onset prcd, clinical signs (or even eye changes) may not be seen until the dog is 4 years of age or older. Most frequently night blindness is the first clinical sign, but then as the condition progresses the dog shows decreased and, eventually, total loss of all vision. Owners may also notice that the dog has dilated pupils and an increase in the shininess at the back of the eye. Some dogs may also develop cataracts secondary to the PRA, seen as an increased cloudiness in the eye.

Since the ophthalmologic and clinical signs of Generalized PRA may not be detected until the dog is 4 years of age, or older, there have been considerable efforts made to find the gene(s) responsible for this condition, and with some success, in a number of breeds. Through genetic research it has been found that there are several different types of prcd with different genes and/or different mutations responsible in the different breeds. Thus a DNA test for PRA in one breed may not be helpful for PRA in another, even though the condition looks the same clinically. Since Malamutes have had a very small number of cases recorded, there is currently no impetus to develop a DNA test for Malamutes.


Known incidence of PRA in Malamutes:

North America: CERF has recorded 2 cases of Generalized PRA in Malamutes (up to end 1999),
Europe: Two cases of Generalized PRA have been recorded in Malamutes under the Swedish Kennel Club's official eye-testing scheme (up to end 2004).

The AMCA health survey conducted in 1996 by Jocelynn Jacobs-Knoll, DVM, recorded 3 cases of PRA and 4 cases of "Retinal Atrophy". This survey had respondents from USA, Canada and At Large (International).


Internal Article

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Offsite References

(Links below will open in new window)

PRA Today -
by Gregory M. Acland, B.V.Sc., D.A.C.V.O., M.R.C.V.S., Center for Canine Genetics & Reproduction, Cornell University
Current research in Progressive Retinal Atrophy, as well as detailed information of all aspects of this disease.   
prcd-PRA Test - Optigen
Describes the method of DNA testing for PRA, and includes information about the different forms of PRA
  prcd-PRA Test - More from Optigen
Describes the method and breeding strategies for the breeds for which DNA testing for prcd-PRA is currently available.
Progressive Retinal Atrophy - Canine Inherited Disorders Database
University of Prince Edward Island, Canada
Gives detailed information about the different types, diagnosis and breeding recommendations for affected dogs. Specifically mentions hemeralopia in the Alaskan Malamute.
Progressive Retinal Atrophy -
by Catherine Marley
Details the similarities and differences of PRA in different breeds.
  Progressive Retinal Atrophy - Veterinary Medical Database
by Julie Gionfriddo, DVM, AVCO Genetics Committee/CERF Liaison
Article from the Purdue University web site, dated June 1998.

 Please check our "Links" page for some personal web sites pertaining to this subject, and stories of affected dogs and their owners.

 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.

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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.

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 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.

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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.

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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.

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causes uveitis and chorioretinitis

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causes uveitis and chorioretinitis

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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.

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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.

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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.

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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.

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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.

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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.

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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).

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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

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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.

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Outflow System: Most common clinical sign is epiphora.

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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

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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).

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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.


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

Statement / BY-Line

Anchor Jump Menu:
Aqueous Humor Pathologic Effects Types Clinical Signs Tonometry
Treatment Medical Therapy Surgical Therapy Ciliary Body Destruction  

Aqueous Humor Dynamics and Intraocular Pressure

Aqueous humor is produced in the ciliary body by active secretion and ultrafiltration of plasma. The enzyme carbonic anhydrase participates in the energy-dependent secretory phase of aqueous production. Most of the aqueous humor flows from the posterior chamber, through the pupil, to the anterior chamber, and exits at the iridocorneal angle into the intrascleral venous plexus. A small percentage of the outflow in dogs and cats (uveoscleral or nonconventional) also exits through the iris, ciliary body, choroid, and sclera. The balance between formation and drainage of aqueous humor maintains intraocular pressure (IOP) within a normal range of 15 to 25 mm Hg.

By definition, glaucoma is increased IOP with associated visual deficits. In most cases in dogs and cats, glaucoma is caused by obstruction of the aqueous humor outflow pathways. It remains a challenge to the veterinarian to detect the early subtle disturbances of glaucoma and to effectively treat this condition. Delayed or inadequate therapy can lead to irreversible blindness and a painful, cosmetically unacceptable eye.

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Pathologic Effects of Glaucoma

All ocular tissues are eventually affected by the elevated IOP. The presence, individually or as a group, of a "red eye," corneal edema, mydriasis, blepharospasm, blindness, and buphthalmos can be explained by the increased IOP. If the IOP cannot be reduced, an overall increase in the size of the globe may result (buphthalmos). This change may occur more rapidly in young dogs and cats. Ruptures of the cornea's inner limiting (Descemet's) membrane may accompany the elevated corneal tension and buphthalmos to produce multiple, linear corneal striae. Persistent corneal endothelial damage can result in corneal edema. Buphthalmos causes increased tension on the lens zonules. Zonular disinsertion results in lens subluxation or luxation.

Pupillary light reflexes may be normal, slow, or absent in early glaucoma, depending on the functional status of the iris sphincter muscle, retina, and optic nerve. Acute elevation of IOP (greater than 45 mm Hg) causes paralysis of the iris sphincter and dilator muscles. Prolonged or recurrent elevations of IOP lead to degeneration of the retina and optic nerve, with excavation or cupping of the optic nerve head.

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Types of Glaucoma

Glaucoma is divided into primary (including congenital) and secondary categories. The iridocorneal angle may be open, narrow, or closed in either type. Abnormal development of the iridocorneal angle (goniodysgenesis) has been noted in some breeds. Evaluation of the iridocorneal angle is performed with gonioscopy in the dog but may be performed with focal illumination in the cat.

Primary glaucoma in dogs is a breed-related, hereditary condition. Predisposition to primary open-angle glaucoma in the Persian and Siamese cat breeds has also been noted, but in the author's experience, domestic short-hairs are more often affected. In both dogs and cats, affected animals may present with only one eye involved, but the risk is very high for development of glaucoma in the other eye.

Secondary glaucoma is more commonly encountered than primary glaucoma in dogs and cats. The elevated IOP results from other disease processes within the eye. The glaucoma may be open or closed angle, and in some instances is associated with pupillary block. The condition tends to be unilateral without an inherited basis.

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Clinical Signs of Acute and Chronic Glaucoma

Lens lux with ciliary process
Figure 11
Lens lux with ciliary process
Optic nerve atrophy with cupping CN
Figure 12
Optic nerve atrophy with cupping

The presentation of a patient with a painful, red eye requires that glaucoma be ruled out among the possible diagnoses of conjunctivitis, uveitis, or keratitis. Pain manifested as depression, anorexia, rubbing at the eye, and squinting is common. Congestion of episcleral vessels, diffuse corneal edema, a fixed and dilated pupil, and blindness will occur as the IOP increases. The onset of clinical signs in cats is often insidious, as cats are less likely to demonstrate the acute intense corneal edema and episcleral congestion exhibited in dogs. Signs of chronic glaucoma are dramatic. They include combinations of the early signs with buphthalmos, lagophthalmos, exposure keratitis, luxated lens, corneal striae, optic nerve atrophy with cupping, and retinal atrophy (Figure 11 and 12).

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IOP must be accurately measured to diagnose glaucoma. The normal canine and feline IOP is 15 to 25 mm Hg. An IOP greater than 30 mm Hg is considered pathologic and diagnostic for this condition. It is possible to crudely evaluate IOP digitally if the IOP is very high or low, but this is not satisfactory to evaluate clinical response to therapy. The Schiotz's indentation tonometer allows the practitioner to diagnose and evaluate treatment in small animals with glaucoma. The human Schiotz table is accurate for the dog. The Tonopen applanation tonometer has made it much easier to diagnose and treat the animal glaucomas.

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The objectives of therapy are to maintain vision and eliminate pain by (1) increasing aqueous outflow, (2) decreasing aqueous production, and (3) preventing or delaying glaucoma in the other eye. Primary glaucoma may be more difficult to control than secondary glaucoma because it is eventually bilateral, and blindness is a possible sequela despite therapy. I nevertheless recommend prophylactic therapy for the unaffected eye in animals afflicted with unilateral primary glaucoma. In secondary glaucoma, the inciting cause is identified and either removed or suppressed. Topical corticosteroids may be indicated to diminish inflammation when nonseptic anterior uveitis is also present.

Medical therapy is the treatment of choice in animals with a history of acute primary or secondary glaucoma. Treatment should be instituted to reduce the IOP as soon as possible to alleviate pain and preserve vision. Animals presented with a history and clinical signs of chronic glaucoma should be considered for medical and surgical therapy. The iridocorneal angle gradually closes in most types of glaucoma and the initially effective treatment becomes inadequate. Surgery is the only option available when vision continues to diminish in spite of maximum medical therapy.

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Medical Therapy

Multiple drug therapy to decrease IOP by reducing production of aqueous humor and diminishing the resistance to aqueous humor outflow is the most effective approach.

Treatment of the ocularly normotensive eye in a purebreed dog with apparently unilateral glaucoma can delay the onset of overt ocular hypertension in the second eye a median of 30 months. Betaxolol and demecarium were each effective at delaying onset of glaucoma in dogs when administered topically.

Carbonic-anhydrase inhibitors reduce ciliary-body production of aqueous humor independent of diuresis. These drugs can cause metabolic acidosis, and the dosage should be carefully adjusted to minimize side effects, which include panting, nausea, and vomiting. Non-carbonic anhydrase-inhibiting diuretics do not significantly reduce IOP!

Topical parasympathomimetic drugs act primarily to cause ciliary muscle contraction, increasing the outflow of aqueous humor. This action is independent of their effect on the iris sphincter muscle. Parasympathomimetics are contraindicated in glaucoma associated with anterior uveitis. They should be used with caution in glaucoma associated with anterior lens luxations. Sympathomimetic drugs reduce IOP by increasing production of aqueous humor and increasing outflow. These drugs are most effective in reducing IOP when combined with parasympathomimetics. ß-adrenergic antagonists decrease production of aqueous humor, but the specific mechanism of action is not known. The ocular hypotensive effects are additive to those of carbonic-anhydrase inhibitors and parasympathomimetics.

Oral and intravenous hyperosmotic agents lower IOP rapidly by osmotically reducing the volume of the vitreous. They are used in the emergency treatment of acute glaucoma but are ineffective or impractical for long-term or maintenance therapy.

Intravitreal glutamate levels are elevated in canine glaucoma. Glutamate is extremely toxic to the retinal ganglion cells. It overstimulates them. Glutamate excitotoxicity is mediated by intraneuronal calcium influx. Intraneuronal homeostatic imbalance induces apoptosis and cell death. The use of glutamate receptor antagonists and calcium channel blocking drugs to protect the retina and optic nerve is being studied.

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Surgical Therapy

Surgical procedures are divided into those that increase aqueous humor outflow and those that decrease aqueous humor production. Surgery should be considered when the IOP cannot be controlled medically, especially when vision is still present. Anteriorly luxated lenses should be removed in functioning eyes to relieve pupillary block and prevent corneal damage due to the lens touching the corneal endothelium.

Cyclocryotherapy has been found to be effective in decreasing production of aqueous humor by the transcleral freezing of the ciliary body with nitrous oxide. This may require repeated applications for optimal IOP control.

The YAG laser is preferred over nitrous oxide by the author to cause ciliary body necrosis (cyclophotocoagulation). The eye is less irritated postoperatively and the IOP stays low for longer periods of time. Only 6% of dogs with cyclophotocoagulation will still be visual at one year after installation.

Gonioimplant. Several types are available to passively shunt aqueous humor to the subconjunctival space. They tend to fail by fibrosing shut in dogs. Only 18% of dogs with gonioimplants will still be visual at one year after installation.

Enucleation or evisceration with prosthetic silicone implants is indicated when vision is lost in uncontrolled glaucoma. The source of pain is removed, and no further medication is necessary. The cosmetic appearance of the prosthetic implant is sometimes preferred to that of enucleation. Prosthetic implants should not be used when glaucoma is or may be associated with intraocular infection or neoplasia.

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Vitreous Aspiration and Pharmacological Ciliary Body Destruction

Vitreous aspiration and pharmacological destruction of the ciliary body by intravitreal injection of gentamicin combined with dexamethasone has been used for the management of chronic glaucoma. This procedure may be indicated in permanently blind glaucomatous eyes without intraocular neoplasia or infection.


Table 1: Pharmacologic Agents for

Medical Treatment of Glaucoma

Carbonic-anhydrase inhibitors (oral)
  1. Acetazolamide (Diamox, Lederle): 10 to 25 mg/kg divided 2 to 3 times daily

  2. Dichlorphenamide: 10 to 15 mg/kg divided 2 to 3 times daily

  3. Methazolamide (Neptazane, Lederle): 5 mg/kg divided 2 to 3 times daily

Parasympathomimetics (topical)
  1. 1 to 2% pilocarpine every 6 hours

  2. 0.125 to 0.25% demecarium bromide: 1 to 2 times per day

Sympathomimetics (topical)
  1. Brimonidine 0.2%: 2 to 3 times per day

Beta-adrenergic antagonists (topical)
  1. 0.5% timolol maleate (Timoptic, Merck): 2 to 3 times per day
    Timolol may precipitate or aggravate feline asthma due to systemic absorption and bronchoconstriction.

  2. betaxolol (0.5%) (Betoptic, Alcon, Ft Worth, TX): 3 times per day.

Hyperosmotics (parenteral)
  1. 20 % mannitol: 1 to 2 mg/kg IV; repeat in 6 hours if necessary

  2. 50 % glycerol: 1 to 2 mg/kg PO; repeat in 8 hours if necessary

Topical Carbonic-anhydrase inhibitors
  1. Dorzolamide (2% Trusopt, Merck): 1 drop TID

  2. Brinzolamide (1%), Azopt, Alcon, Ft Worth, TX: 1 drop TID

Topical Prostaglandins
  1. Latanaprost 0.005%, Pharmacia, 1 drop BID

  2. Travaprost (Travatan; Alcon) 0.004% BID

  3. Bimatoprost (Lumigan; Allergan) 0.03% BID

Calcium Channel Blockers
  1. Norvasc, amlodipine. 0.625 mg/10 lbs PO SID


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.


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

Current Concepts in Veterinary Ophthalmology - November 1, 2003

Anchor Jump Menu:
The Cornea Ulcerative Keratitis Classification Diagnosis  Treatment
 Corneal Erosion  Lacerations  Bullous Keratopathy    


The cornea is the most powerful refractive surface of the eye; it supplies 70% of the eye's refractive or light bending power. The cornea is also an extremely strong tissue. It is transparent so that light rays can enter the eye. Transparency is maintained by several anatomic mechanisms: 1) lack of blood vessels; 2) lack of pigment; 3) non-keratinized anterior surface epithelium; 4) precise organization of the stromal fibrils; 5) small size of the stromal fibrils; 6) relatively dehydrated compared to sclera.

Most domestic animal species have 4 corneal layers. The outermost stratified squamous epithelium has 3 cell types (superficial squamous cells, wing cells, and basal cells). This layer is a barrier to the precorneal tear film. A basement membrane is secreted and attaches to stroma. The stroma constitutes approximately 90% of the corneal thickness, and it is relatively acellular (mostly collagen). Descemet's membrane is the basement membrane secreted by the corneal endothelium. It is produced throughout life, and therefore the thickness increases with age. It is about 14 µm thick! The innermost endothelium is only 1 cell layer thick, and contains a sodium ATPase pump. This feature is very important in maintaining corneal transparency, as the pump helps to keep the stroma relatively dehydrated.

Most of the corneal nerves are concentrated superficially. They are branches of the trigeminal nerve, and form a very dense anterior sensory neural network. The cornea is actually one of the most sensitive tissues in the body. There are no nerves in Descemet's membrane. The corneal thickness varies by species. It is often thinner centrally than peripherally, depending on the species. The average thickness of the central dog cornea is 0.6 mm; in the horse the central cornea is approximately 1 mm thick.

Limbus and Sclera

The limbus is located at the peripheral edges of the cornea. It is about 1 to 1.5 mm wide, and forms the transition zone between the cornea and sclera. The epithelium of the cornea merges with the bulbar conjunctival epithelium in this area. The sclera constitutes the major portion of the outer fibrous tunics (5/6). The equator is the thinnest region in most species.

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The most important disease of the cornea

Ulcerative keratitis (corneal ulceration) means that the corneal epithelium and possibly varying amounts of underlying corneal stroma are missing. In simple traumatic corneal injuries in which a small amount of epithelium is absent, healing is rapid. Normal corneal epithelium is a very effective barrier against invading bacteria. If the ulcer becomes infected or the epithelium is unable to attach to the underlying stroma, healing is delayed.

07 fungalFigure 7
Chronic or infected ulcer

In chronic or infected ulcers, proteases and collagenases digest protein and collagen of the stroma (Figure 7) and may greatly speed the progression of an ulcer to a descemetocele (Figure 8), rupture of the cornea, and then to iris prolapse (Figure 9) (within 12-48 hours in some cases).

Corneal dissolution and liquefaction under the influence of proteases is often referred to as "melting". Ulcers in which proteases are active have a grayish-gelatinous liquefied appearance around the ulcer margin which must be distinguished from corneal edema.

Ulcerative keratitis is the most serious ocular disease for veterinarians. Regardless of the initial cause, all ulcers have the potential to progress to endophthalmitis if not treated.

08 descemetoceleFigure 8
Descemetocele ulcer

09 lensruptureFigure 9
Lens rupture

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Superficial ulcerations or abrasions should heal rapidly if they do not get infected. They can be traumatic in origin. It has been shown that normal horse corneal epithelium migrates at 0.6 mm per day. We guess that the dog and cat are similar or faster.

The following types of ulcers will be covered in detail: recurrent superficial corneal erosions; deep stromal ulcers; fungal keratitis; descemetoceles; perforating ulcers (iris prolapse); and corneal lacerations (superficial and full-thickness).

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There are multiple causes of corneal ulcers. Corneal ulcers can result from mechanical causes such as traumatic abrasion; corneal or eyelid foreign bodies; and eyelid anomalies (entropion, distichia/districhiasis, ectopic cilia, and trichiasis)

Infectious etiologies also cause corneal ulcers. Infectious organisms can be bacterial, fungal, or viral. Culture and sensitivity are important diagnostic tools to use with infectious ulcers.

Keratoconjunctivitis sicca (KCS or "dry eye") can result in corneal ulceration. This is especially true with cases of acute onset KCS, in which corneal ulceration can occur rapidly and progress quickly. Ulcers are less common with chronic KCS.

Bullous keratopathy results in rupture of epithelial bullae that form with chronic corneal edema. Ulcers result from the rupturing of the bullae. These ulcers can range in size from small to very large and are variably painful. This is a devastating disease in the cat.

Exposure keratitis can result from either neuroparalytic disease (facial nerve paralysis, resulting in an inability to blink) or from neurotrophic disease (paralysis of ophthalmic branch of trigeminal nerve; corneal sensation is important to healing of corneal ulcers).

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A. Clinical Signs

The majority of animals with corneal ulcers present with pain as evidenced by blepharospasm. Corneal sensation is one of the major protective factors that the eye exhibits. Corneal sensory nerves are located mostly in the superficial cornea, and the nerves lose their myelination as they cross from the periphery into the center of the cornea. An "axon reflex" is thought to exist in the cornea such that when corneal touch and pain receptors are stimulated, miosis of the pupil, hyperemia, and increased protein levels in the aqueous humor occur. The axon reflex is responsible for the clinical signs of anterior uveitis observed with painful corneal conditions. These results appear to be mediated by prostaglandins, histamine, acetylcholine, and possibly substance P. Other clinical signs seen commonly with corneal ulceration include epiphora, photophobia, and corneal edema, causing a change in transparency. IT IS IMPORTANT TO REMEMBER THAT UVEITIS ALWAYS EXISTS WITH CORNEAL ULCERATION.

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B. Diagnostics

Culture and sensitivity should be performed routinely when an ulcer is infected or "complicated." Not all small animal ulcers need to be cultured the first time you see the patient. However, if the corneal ulcer appears to be "melting" or if the ulcer has not responded to proper treatment, these ulcers should be cultured.

Schirmer tear test and/or phenol red thread test should be performed on all canine patients presenting with corneal ulceration. A large percentage of dogs with dry eye with initially present with corneal ulceration. An eye with an ulcerated cornea should have excessively high tear production resulting in epiphora. If the Schirmer tear test value is in the normal range or similar to the normal fellow eye, then KCS should be suspected.

Cytology can be performed using topical anesthetic. Remember to collect culture samples and perform Schirmer tear tests prior to applying topical anesthetic, as the anesthetics can interfere with interpretation of results.

ALL ulcers should be stained with fluorescein and sometimes with rose bengal. Fluorescein stain (which is hydrophilic) will adhere to exposed stroma, but will not stain epithelium or Descemet's membrane. Rose bengal is used to evaluate mucin tear layer defecnts, and devitalized epithelium that is still attached but not healthy.





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A. There are multiple steps in the treatment of a corneal ulcers. The deeper the ulcer, the more aggressive is the medical and likelihood of surgical therapy. The first step is to determine the etiology, and remove or eliminate the specific cause. This means evaluating the eyelids and eyelashes, tear production, corneal culture, and corneal cytology.

B. Broad-spectrum antibiotics are usually administered; culture and sensitivity tests can guide selection in recurring, non-healing, or infected ulcers. Effects of in vitro antibiotics on k9 corneal epithelial cells: chl<tobr <npg <gent <cef<cipr (Hendrix AJVR 62:1664-1669, 2001).

C. Prevention of collagen breakdown and ulcer progression are also important steps. Collagenases and proteases are derived from leukocytes in the tears and can be powerful in the destruction of corneal stroma. There are several drugs that can be used to help inhibit protease activity:

Autologous Serum and/or 0.05% EDTA

Serum contains an alpha-2 macroglobulin with anticollagenase activity. Blood is drawn from the patient or an animal of the same species, spun down, and serum drawn off and stored in the refrigerator in a dropper bottle or serum tube for up to 14 days. It should not be stored at room temperature, but the dose about to be given can be warmed to room temp immediately before administration. Serum is non-toxic, and should be used as many times a day as possible.a

EDTA (0.17%)

can be given several times a day as well. Acetylcysteine (5-10%) is used topically for its collagenase and protease inhibiting properties. Acetylcysteine is unstable at room temperature, so the solution must be kept refrigerated. Frequency of treatment is decreased from every 1 to 2 hours for the first few days to 3 or 4 times daily for the next 7-10 days.

D. Treatment of accompanying anterior uveitis is also important with corneal ulceration. Topical 1% atropine is usually instituted to relieve ciliary spasm and pain (CYCLOPLEGIA) due to secondary anterior uveitis, and to decrease the formation of synechiae from the miotic pupil (as a result of uveitis). Be careful as it can cause a temporary KCS in small animal patients.

Topical NSAIDs can be used to treat ulcer induced uveitis in some cases.

E. In the treatment of deep corneal ulceration or descemetoceles, provision of corneal support is important. Coverage with one of the various kinds of conjunctival flaps should be maintained for 10-21 days. Types of conjunctival flaps include: 360 degree, hood, island, pedicle, and bridge.



A. Synonyms 

include Boxer ulcer, indolent ulcer, persistent ulcer, rodent ulcer, refractory epithelial erosion, recurrent corneal erosion syndrome. Middle to old age groups are most commonly affected, and there may be an increased incidence in females. Breed predilection has been demonstrated in the Boxer, Corgi, Pekingese, and Lhasa Apso, but refractory ulcers have been documented in more than 24 breeds of dog. History, signalment, and ophthalmic findings are all important in the diagnosis of refractory corneal ulceration.

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B. Pathogenesis

Refractory corneal ulcers in the dog are usually primary. However, they can also be seen secondary to eyelash or eyelid abnormalities, corneal edema, infection, or tear film abnormalities. It is important to rule out conditions that can secondarily cause indolent ulceration in order to successfully treat the syndrome.

10 ulcer

Figure 10
Superficial corneal ulceration with
overlying lip of unattached
epithelium and
fluorescein staining

The specific pathogenesis of refractory ulcers is still not known. Normally the corneal epithelium attaches to the underlying stroma via hemidesmosomes in the basal epithelial cell membrane. Some animals with refractory corneal ulcers have been shown to have fewer hemidesmosomes as well as abnormalities in the epithelial basement membrane. Histologically, there are focal areas of epithelial separation with splitting of the basement membrane, and edema (in and between the basal cells) with accumulation of a basement membrane-like material.

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C. Clinical Signs

Variable pain (manifested by tearing, blepharospasm, photophobia) is present, and there is no history of traumatic injury. On ophthalmic examination, a superficial corneal ulceration with an overlying lip of unattached epithelium around the edge of the erosion is evident (Figure 10). The use of fluorescein staining will illustrate the ulcer bed as well as reveal the degree of unattached epithelium as the underlying stroma will take up stain.

D. Differential Diagnoses Causes for persistent ulcer:

KCS, ectopic cilia, foreign bodies, entropion, infection

E. Treatment

1. Debridement of unattached and loosely attached epithelium is essential. Topical anesthetic and dry cotton-tipped applicator are used to remove abnormal epithelium. Superficial grid keratotomy (GK) or multiple punctate keratotomy (MPK) have revolutionized the treatment of indolent ulcers. Animals require only topical anesthesia, or rarely light sedation. A 20 gauge needle is used to make cross hatches ("tic tac toe") through the ulcer bed with the scratches approximately 1-2 mm apart into adjacent normal epithelium and stroma (GK) or multiple punctures into the anterior stroma (MPK) and adjacent 1-2 mm of epithelium. Both techniques have been shown to increase the healing rate of refractory ulcers. Superficial keratectomy has been shown to be very effective, especially in terms of decreasing recurrences. This requires more specialized equipment and magnification.

Chemical removal of the epithelium can also be accomplished with dilute topical povidone iodine or phenol.

2. Refractory ulcers are treated medically following debridement and possible keratotomy with the some or all of the following mechanisms. Topical broad spectrum antibiotic solutions (triple antibiotic or chloramphenicol; do not use gentamicin!!) 2-4 times per day; topical cycloplegic (1% atropine) as needed; topical hyperosmotic agent (2-5% NaCl solution) to decrease edema; bandage soft contact lens or collagen shields; Elizabethan collar to prevent self trauma; 0.2% sodium hyaluronate may also be beneficial topically [Adequan (100 mg/ml) for topical use: 50 mg/ml in polyvinyl alcohol artificial tears TID (Tears Naturale)]; and the growth factor in serum may be beneficial in persistent erosions.

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The management depends on the depth of laceration. All should be stained with fluorescein to help assess the depth and affected area of the laceration. Superficial lacerations are treated as "simple" ulcers (topical antibiotics and atropine). Deep, non-perforating lacerations are treated more aggressively. Topical broad spectrum antibiotics and 1% atropine are used. If the laceration is judged to be less than ½ thickness, treat as simple ulcer; if more than ½ thickness, suture cornea and place conjunctival flap.

Perforating (full thickness) lacerations are emergencies. Animals require systemic antibiotics, general anesthesia and surgical repair of cornea; topical antibiotic solution (not ointment), topical atropine solution, and surgical repair. This entails repositioning or amputating protruding iris, reforming the anterior chamber with Lactated Ringers, and suturing the corneal with #7-0 or #8-0 absorbable suture material. A conjunctival flap is also placed if needed.

If iris prolapse has occurred more than 2-6 hours earlier, and the iris appears nonviable, it should be amputated using cautery. The cornea should then be sutured as above.

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Chronic corneal edema leads to formation of small vesicles in the corneal epithelium that coalesce into larger bullae which may rupture, causing loss of epithelium and corneal ulceration. It is most common in cats. Treatment: Remove underlying cause; support cornea (nictitans flap and/or possibly a tarsorrhaphy prior to bullae rupturing); topical antibiotic and atropine 1%; topical hypertonic NaCl ointment or solution; corneal transplantation.

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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.


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


The examination of the eye and periocular structures is essential for the complete evaluation of the patient. The diagnostic equipment needed for the basic ophthalmic examination is readily available to the general practitioner. Discussion of the more specialized procedures such as slit lamp biomicroscopy, ultrasonography and electroretinography will also be included to familiarize you with what is available should you need to refer a patient to a veterinary ophthalmologist.

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A. Vision evaluation

The animal should be observed walking into the examination room with the client, or in its own environment. A blind animal may exhibit high stepping, collision with objects, a stare-like expression, or reluctance to move in a strange environment. The owner's impression that the animal "sees" well at home must be interpreted cautiously. Animals can "memorize" their own environment. The animal is permitted a few minutes to adjust to the room and observed as the history is obtained.

The patient's vision can be further evaluated by noting the response to hand movements, bright lights or to cotton balls tossed into the visual field. The menace response and the visual placement reaction can also be performed to evaluate the vision. In certain circumstances, each eye should be evaluated separately by patching one eye with a bandage or by covering it with one hand.

The vision examination should be performed in normal light, then in dim light. If you can see the cotton balls or the obstacles of the maze test, the dog or the cat should be able to see them better than you since their night vision is more developed than ours. Cats generally do not menace test well, but respond well to bright light stimulation, laser lights, and cotton ball testing.

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B. Ocular examination

Following an evaluation of vision the need for special diagnostic tests is determined. An orderly sequence of diagnostic tests must be followed based on the special requirements of each test. Evaluation of the tear film (Schirmer tear test) must be done before the eye is manipulated or any drugs are instilled. Cultures of the external ocular structures must be done before extensive cleaning is done and before drugs are instilled. The use of mydriatics is necessary for examination of the lens and posterior segment, but should not be given prior to measuring the intraocular pressure (IOP). The intraocular pressure evaluation requires topical anesthetic and must be recorded before excessive manipulation or before the patient becomes restless and excited.

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1. Periocular examination: Orbit and adnexa

Examinations of anatomic structures should begin with the orbit and other periocular tissues. Orbits are evaluated for symmetry, eye-orbit relationship, deformities or enlargements. Because of marked variations in eye position of different breeds, one should be acquainted with the various breed characteristics. The extremes of variation in eye position can be represented by the relative enophthalmia of the collie and the exophthalmia of the Pekingese.

The presence or absence of strabismus and nystagmus is noted. Esotropia (crossed-eyes) is inherited in Siamese cats but in dogs may represent severe intraocular or neurological disease. Nystagmus occurs frequently in Siamese, apparently not always associated with clinically detectable vision defects, but in dogs may result from congenital intraocular diseases, or acquired vestibular or cerebellar diseases.

The eyelid position may be helpful in determining relative globe size. Looking from over the top of the animal's head helps to estimate globe position. Additional evaluation of the orbit consists of examination of the mouth (floor of the orbit), palpation of orbital rim, retropulsion of the globe, and evaluation of nasal patency, if necessary.

Special examinations such as standard skull radiography, orbital angiography, ultrasonography, CT and MRI, and surgical exploration may be necessary for a thorough evaluation.

*** MAGNIFICATION is extremely important to indentify impacted meibomian glands, ectopic cilia, distichia, corneal vessels and other subtle changes. A simple otoscope head with a magnifying lens and bright light source works great. Other magnifying glasses or headloupes are also available.

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2. Eyelids

The eyelids are examined for abnormalities of position, function and structure such as lagophthalmos, ptosis, trichiasis, ectropion, entropion, blepharitis, lid neoplasms, etc..

The blink reflex should be evaluated. The efferent limb of this reflex requires the integrity of the facial nerve (CN VII) and the orbicularis oculi muscle. The afferent limb may be a menace (CN II), corneal sensation (CN V) or touch sensation to the periorbital skin (CN V). Rapidity and completeness of the blink should be evaluated.

The lower and upper eyelids should touch the globe. Lower lid-globe contact is important to prevent accumulation of tears and debris. The lower "lacrimal lake" may be grossly distorted by anesthetics and tranquilizers. Cilia or eyelashes occur mainly on the dog's upper lid in three irregular rows. The lower eyelids of dogs and both eyelids of cats are usually void of cilia. The eyelid contours are regular and gently curved, partially exposing the openings of the tarsal or Meibomian glands (gray line). The duct orifices are frequently raised and nonpigmented. Aberrant cilia (distichia) may emerge from the spaces among the Meibomian gland ducts, or the actual duct orifices. Ectopic cilia emerge from the within the palpebral conjunctiva of the upper lid and are frequently the same color as the dog's hair coat. They can escape detection without careful examination.

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3. The Conjunctiva and the Nictitating Membrane

The palpebral conjunctiva is examined by manual eversion of the upper and lower eyelids. Excessive lymphoid follicles, increased vascularity, foreign bodies, ectopic cilia, obstructed tarsal glands, hemorrhage, lacerations, abnormal growths and edema (chemosis) may be abnormalities observed. Coloration of the conjunctiva can be used to assess the presence of anemia and icterus. Because the palpebral conjunctiva is transparent, chalazia or impacted Meibomian glands appear as slightly raised yellow masses.

Examination of the palpebral (outer) and bulbar (inner) surfaces of the nictitans is important for diagnosis of several common external ocular conditions. Frequent abnormalities are eversion of the cartilage of the nictitans, prolapse of the gland (cherry eye), foreign bodies, follicular conjunctivitis, enlargement of the secretory gland, foreign bodies, follicular conjunctivitis, and enlargement of the bulbar lymphoid tissue.

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4. The Sclera

The sclera should be scrutinized for change in color, abnormal masses, and tears or lacerations. Small vessels in the episclera are usually visible and occasionally a large vortex vein (especially the dorsolateral vein) can be seen. Enlargement and congestion of the episcleral veins occur commonly with glaucoma. This venous enlargement remains even after the glaucoma is "controlled". Hyperemia of the episcleral vessels occurs in association with inflammatory conditions. The "ciliary flush" or limbal hyperemia from iridocyclitis is usually less affected by topical phenylephrine while that associated with the conjunctivitis will usually blanch. The perilimbal scleral vessels are small straight and immovable vs larger mobile and branching conjunctival vessels.

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5. The Cornea

Corneal sensitivity (corneal reflex) is tested by a small wisp of cotton gently touched to the cornea. (This must be done prior to topical anesthetic instillation). If the animal sees the stimulation, you will get a false positive.

The cornea is normally transparent, avascular, moist, and unpigmented with a smooth, even contour. It should be carefully examined for loss of transparency (edema or infiltrates), opacity, vascularization, pigmentation, dryness, growths, foreign bodies, lacerations, changes of contour, and ulceration.

Two types of vascularization occur in the cornea: superficial and deep. Superficial vessels occur in the anterior one-half of the corneal stroma, are usually continuous with visible conjunctival vessels, are "tree-like", and associated with external corneal diseases. Deep vessels appear as small, fine vessels in the corneal stroma that extend from the anterior sclera or deeper limbal vessels (paint brush border), and are associated with intraocular inflammation.

Corneal ulcer
Figure 1
A corneal ulcer/erosion

Examination of the cornea is incomplete without utilization of topical ophthalmic stains. Fluorescein is used to demonstrate the presence or absence of corneal ulcers. For topical use, fluorescein impregnated paper strips are preferred to fluorescein solution to insure sterility. Because the water-soluble fluorescein stains the preocular film, a faint green may occur on the corneal surface.

The corneal epithelium is lipid-selective and prevents any appreciable corneal penetration by fluorescein. In the presence of a corneal epithelial defect, the dye rapidly diffuses into the corneal stroma. An area of fluorescein retention by corneal stroma is indicative of an epithelial defect (Figure 1).

Rose bengal is a valuable stain in the evaluation of the health of the corneal and conjunctival epithelium. It produces a brilliant red coloration of any dead or degenerating cells, and indicates defects in the mucin layer of the tear film. Rose bengal is retained by the cornea and conjunctiva in early fungal keratitis, keratoconjunctivitis sicca, pigmentary keratitis, exposure keratitis, viral keratitis, and certain other corneal ulcers.


Aqueous flare in a cat
Figure 2
Aqueous Flare in a Dog

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Increased protein in the aqueous humor, when viewed with a focal light source, gives the appearance of a light beam passing through smoke. This is known clinically as "aqueous flare" and its appearance results from the optical Tyndall phenomenon. Aqueous flare means there is uveitis (Figure 2). When checking for flare also compare the depth of the anterior chamber between the two eyes.

The iris is examined with a focused beam of light and magnification for color, shape, pupil size, surface, and movement. Iridal color in dogs varies from dark brown to blue, and generally 3 "zones" of color are evident (pupillary margin, iris collarette and the iris base). Light brown irides occur in many breeds, such as the Brittany Spaniels, German Short Hair Pointers and other breeds. Iridal heterochromia is not uncommon in white cats, St. Bernards, Great Danes, Beagles, merle Collies, Australian Shepherds, Old English Sheepdogs, Dalmatians and the merle Sheltie. Iris color in cats varies from blue to yellow-green to brown. In acute iritis, the iris may appear congested and swollen with loss of detail, and it may become darker in appearance with chronicity.

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7. The Lens

The lens, which is normally a transparent avascular structure, should be examined for opacities (cataracts), position, presence, and size. Focal cataracts should be localized within the various parts of the lens as prognosis and etiology may be suggested by location. Nuclear cataracts are usually stationary while those affecting the equator or posterior cortex are often progressive. By slit lamp biomicroscopy, the canine lens may contain focal imperfections that are not "cataractous." Early cataract formation, evidenced usually as focal crystallization, vacuoles and water clefts, can be detected long before visual disturbances occur.

Localization of focal cataracts can be performed using the tapetal reflex to highlight the opacity and then observing which direction it moves as the animal's eye moves. For practical purposes, in the dog and cat the center of axis of rotation of the eye is the center of the lens. Thus if a cataract is in front of the lens it will move with the eye movement. If a cataract is in the back of the lens it will move in the opposite direction of the eye movement. Location of a cataract may give clues about its cause i.e. inherited or associated with PRA.

Nuclear sclerosis of the lens begins to develop in dogs around 6 years. Biomicroscopic examinations can detect refractive changes between the lens nucleus and cortex as early as three years of age in dogs. Advanced nuclear sclerosis is clinically evident as a blue zone limited to the lens nucleus that does not impair ophthalmoscopic visualization of the fundus and does not impair vision. This is frequently mistaken for cataract formation in older animals by owners and veterinarians.

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8. The Vitreous

The vitreous humor is normally a clear gel. The anterior portion can be examined using focal illumination and some magnification. The posterior aspect of the vitreous is examined by ophthalmoscopy or the slit lamp biomicroscope with added lenses. Frequently seen vitreous abnormalities include vitreous strands, asteroid hyalosis, hemorrhage and infiltration with inflammatory cells. Small remnants of the hyaloid vasculature (seen as white strands) are frequently encountered behind the central posterior lens capsule in the vitreous immediately posterior to the lens. Liquefaction of the vitreous is called syneresis, and opacities that occur in the liquefied state are called "synchysis scintillans". These opacities often rise and fall in the vitreous as the eye moves.

Differentiation of lens and vitreous opacities may pose a problem for the clinician. Localization of intraocular opacities can be achieved by noting direction of movement in relation to the center of the globe, or by slit lamp biomicroscopy. The first procedure is convenient and assumes the center of rotation of the eye is the posterior aspect of the lens nucleus in the dog. Opacities which are anterior will move with eye movement; for example, an anterior cortical cataract will move left when the eye turns left. Opacities posterior to the center of rotation will move in the opposite direction. In the horse the optical center of the eye is the posterior pole of the lens. The stability of the opacity may also help to differentiate lens from vitreous. Lens opacities are fixed and remain stationary when the eye stops moving. Vitreous opacities tend to move slightly or oscillate within the gel vitreous after eye movement ceases.

9. The Fundus

03 mialation
 Figure 3
04 fundus
Figure 4

The ocular fundus is examined last and requires direct and/or indirect ophthalmoscopy. Although the fundus can be viewed without drug-induced mydriasis, dilation of the pupil greatly facilitates examination of the complete ocular fundus. The ocular fundus is examined for changes in the normal appearance, detachment of the retina, chorioretinal hypoplasia or dysplasia, vascular patterns, attenuation, congestion, hemorrhage, colobomas, scars, alteration in coloration, changes in pigmentation and foci of inflammation. The optic disc should also be examined for size, shape, color, masses, and pits or colobomas. Swelling and inflammation of the optic disc occurs with optic neuritis, which is characterized by blindness. Myelination of the disk must be differentiated from swelling of the disk (Figures 3 and 4).

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II. Special Diagnostic Procedures

A. Pupillary light reflexes (PLRs)

The size of the pupils are evaluated and the direct and consensual pupillary light reflexes are tested. This should be done with a bright light in a dimly lit room. The pupillary light reflexes are affected by the psychic state of the animal, room illumination, age, many topical and systemic drugs and the intensity of the light stimulus. Older animals may exhibit slow and incomplete pupillary light reflexes resulting from atrophy of the iris sphincter muscle. This is common in small dogs, especially poodles. The pupillary margin may have an irregular or scalloped appearance. Incomplete iris atrophy may give an irregular pupil shape.

The rapidity of pupillary light response, extent of miosis and ability to maintain miosis to constant light stimulation are evaluated. The consensual pupillary reflex is normally equal to the direct. The pupillary light reflexes require integrity of retinal neural cells, optic nerves, optic chiasm, optic tracts, midbrain (Edinger-Westphal nuclei), parasympathetic fibers via the oculomotor nerve, ciliary ganglia and the iridal sphincter musculature. The reflex is subcortical and should be considered an evaluation of the retina and optic tracts, not of vision.

Drug induced mydriasis is not used indiscriminately. The instillation of mydriatics is avoided in animals with predisposition to, or overt glaucoma, and lens luxation. Young puppies dilate slowly, often incompletely, and may require multiple drops. Mydriasis produced by darkening the room may permit a cursory but not complete examination of the ocular fundus. 1% Tropicamide (Mydriacyl-Alcon Laboratories) provides mydriasis within 15 to 20 minutes in a normal eye.

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B. Corneo-conjunctival Cultures and Cytology

Corneo-conjunctival cultures and cytology are helpful in the diagnosis and classification of corneal and conjunctival diseases. The procedures are especially valuable in chronic, severe and non-responsive external ocular conditions. The cultures should be done before any administration of drops, since many of the drugs contain bacteriostatic agents. Topical anesthetics are used prior to the collection of cytologic material.

Sterile swabs are used to collect material for culture. The swab should be moistened. The moistened swab is rubbed over the area to be cultured taking care to avoid skin, hair and other nearby structures. Bacterial identification and disc sensitivity tests aid in the choice of antimicrobial therapy.

To obtain a specimen for cytologic examination topical anesthetic is instilled 2-3 times over a few minutes and the animal's head and muzzle are held firmly by the assistant. To obtain a conjunctival scraping, the lower eyelid is everted and the ventral conjunctival surfaces are vigorously rubbed with a stainless steel or platinum spatula. The collected material is distributed onto glass slides. Ideally, conjunctiva should be scraped vigorously enough to obtain basilar cells without inducing hemorrhage. To obtain a smear of exfoliated cells, a moistened dacron tipped applicator is rubbed along the conjunctival cul-de-sac and then rolled on glass slides. The specimens are stained with new methylene blue, Gram's, Wright's, Giemsa's, or modified Sani's methods.

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C. Nasolacrimal System and Tear Production

The nasolacrimal system and preocular tear film are evaluated by considering both the secretory and excretory components.

Schirmer testing
Figure 5
Schirmer testing in a Dog

Schirmer Tear Test

The precorneal tear film is essential in maintaining normal corneal health. Measurement of tear production is an important diagnostic test when deficiency of the lacrimal system is suspected.

The tear-producing system is evaluated qualitatively by examination of the corneal surface for moistness and luster and quantitatively by the Schirmer tear test (Figure 5). The diagnosis of "dry eye" or keratoconjunctivitis sicca (KCS) may be missed if the Schirmer tear test is not routinely used. The Schirmer tear test measures only the aqueous aspects of tears. Currently, aqueous tear production is most commonly measured using the Schirmer tear test.

Schirmer values:

Dog: 21.9 +/ 4.0 mm wetting/minute
Rabbit: 5.3 +/ 2.9 mm wetting/minute
Cat: 20.2 +/ 4.5 mm wetting/minute

Excessive manipulation of the eyelids, topical anesthesia and exposure to other topical and systemic drugs (such as tranquilizers and atropine) are avoided before the test. Increased tear production because of corneal irritation during the test appears to be of little significance in the dog and the cat. The round end of the test paper is bent while still in the envelope and positioned without contamination in the lacrimal lake at the junction of the lateral and middle thirds of the lower eyelid. The animal usually closes its eyelids during the test. After one minute the paper is removed and measured on a millimeter scale on the paper envelope. The STT strip should be left in position for one minute. It is not a linear test, so if you obtain a value of 7 mm/30 seconds this does not mean it will be 14mm/min!!!! If you get an abnormal value <15mm in less than one minute the test should be repeated leaving the strip in for a full minute.

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Phenol Red Thread (PRT)

The Phenol Red Thread Test is a new, fast and equally accurate method to assess tear production.

In the PRT tear test, the thread is 75 mm long and is impregnated with phenol red, a pH-sensitive indicator. A 3 mm indentation at the end of the thread is inserted into the inferior conjunctival sac for 15 seconds. The alkaline tears turn the pale yellow thread red. A test time of 15 seconds is required compared to the 5 minutes needed for the STT in humans or the 1 minute in dogs.

Anesthesia is not necessary for the PRT tear test because the subject has little or no sensation from the thread. It is theorized that the minimal sensation and short test time give a more accurate indicator of the volume of residual tears in the inferior conjunctival sac of the eyes. Mean length of absorption for the PRT tear test in cats is 23.0 mm ± 2.2 mm/15 seconds. The normal range in cats for the PRT tear test is 18.4 to 27.7 mm/15 seconds. In dogs the mean length of absorption using the PRT tear test is 29.7 to 38.6 mm/15 seconds.

Phenol Red Thread test: Wilson Ophthalmic, 923 West State Hwy 152, Mustang, OK 73064; 1-800-222-2020; Zone-Quick Phenol Red Thread, Tear Test 100/box Part No: 060-0000050-00

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Tear Drainage

The excretory component of the nasolacrimal system is evaluated by the presence or absence of medial canthal tearing; passage of fluorescein instilled onto the eye; nasolacrimal flush; catheterization of the entire system, and by dacryocystorhinography. The nasolacrimal drainage apparatus consists of two puncta and canaliculi, a poorly developed nasolacrimal sac and the nasolacrimal duct. The oval puncta are situated in the upper and lower medial eyelid margins about 1 to 2 mm in the palpebral conjunctiva. A partial to complete ring of pigment may surround the puncta and facilitates their detection.

Passage of fluorescein from the eye to the external nares is a reasonable test for patency of the nasolacrimal system. A strip of fluorescein is moistened with a few drops of sterile eyewash and touched to the upper bulbar conjunctiva. The dye usually appears at the external nares in 3 to 5 minutes. Both sides should be performed at the same time to compare passage times. Ultraviolet light enhances detection of the dye. Fluorescein passage in brachycephalic dogs and is not reliable as the dye may exit more readily into the nasopharynx. The animal's tongue and saliva should be examined with a UV light in these cases.

The nasolacrimal flush determines patency of the system and the treatment of many of its disorders. The upper punctum is cannulated with a 22-23 g blunt lacrimal needle or 22-24 gauge teflon catheter under topical anesthesia. Tranquilization or general anesthesia is seldom necessary for the dog but often necessary for the cat. A 2 to 3 ml plastic syringe with sterile saline is used to inject the solution through the upper punctum, canaliculus, nasolacrimal sac, lower canaliculus and out the lower punctum. Once this "arc" is established, the lower punctum is compressed digitally and the solution is forced through the nasolacrimal duct and out the external nares. If the dog's head is positioned upward, the dog will swallow or gag on the solution. Excessive pressure should be avoided to minimize the danger of rupturing the N-L system above an obstruction.

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D. External Ophthalmic Stains


Examination of the cornea is incomplete without utilization of topical ophthalmic stains. Fluorescein is used to demonstrate the presence or absence of corneal ulcers. For topical use, fluorescein impregnated paper strips are preferred to fluorescein solution to insure sterility.

Rose Bengal

Rose bengal is retained by the cornea and conjunctiva in keratoconjunctivitis sicca, early fungal keratitis, pigmentary keratitis, exposure keratitis, viral keratitis, and certain other corneal ulcers.


E. Intraocular Pressure Measurement (Tonometry)

06 tonopenFigure 6
Tonopen test

Intraocular pressure (IOP) is estimated digitally, and measured by Schiotz tonometry or applanation tonometry. Subtle elevations in intraocular pressure, repeated measurements of glaucomatous eyes under medical treatment, or after surgical intervention require instrument tonometry.

Applanation tonometers (especially the Tonopen type) are very accurate and easy to use. Applanation tonometers are becoming more common in practices (Figure 6). The Tonopen applanation tonometer has made it much easier to diagnose and treat the animal glaucomas.

IOP is 16.8 ± 4.0 mm Hg in dogs; 20.2 ± 5.5 in cats; and 23.2 ± 6.9 in horses.

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F. Ophthalmoscopy

Direct Ophthalmoscopy

Direct ophthalmoscopy is used more frequently by practitioners than indirect ophthalmoscopy. However, both techniques have advantages that complement each other when used together. The method is termed "direct" because a condensing lens is not interpositioned between the ophthalmoscope and the patient's eye. The examiner has a direct optical image of the patient's eye. The fundus image is real, upright and approximately about 17 to 19 times magnified in dogs and cats. The fundus area visualized is about 10 degrees or approximately 2 disc diameters.

In performing ophthalmoscopy, the patient's body and head are minimally restrained by an assistant. The examiner holds the muzzle and/or lids with one hand and with the other hand holds the ophthalmoscope to make the necessary diopter changes. It is preferred to view the tapetal fundus several inches from the patient and then move to 1 to 2 inches from the patient's eye when the optimum focus is achieved and the animal has adapted to the restraint. The diopter setting is usually started at "0" and adjusted to between +3 to -3 diopters to provide the sharpest image possible. By using more positive lenses the lens can be seen at +8 to +12 diopters and the cornea at +20 diopters.

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Indirect ophthalmoscopy

Indirect ophthalmoscopy complements direct ophthalmoscopy. To perform indirect ophthalmoscopy a fairly bright light source is directed into the eye. A condensing lens is interposed between the light source and the eye. Incident light is condensed to illuminate the fundus. The reflected light then is condensed by the same lens to form a virtual, inverted, and reversed image between the lens and the light source.

The advantages of binocular indirect ophthalmoscopy are penetration of cloudy media, large field of view (hence an excellent survey instrument), examination of the peripheral fundus, ease of compensation of refractive errors and eye movements, stereopsis, greater distance between examiner and patient, two to three simultaneous observers and the ability to readily examine the more intractable patients with less hazard to the examiner. The disadvantages include less magnification for studying particular areas, and the need for drug-induced mydriasis.

Indirect ophthalmoscopy can be employed with only a light source and a lens. Several commercial indirect ophthalmoscopes are available. Regardless of the light source used, the power and type of lens used determines the ease and accuracy with which the fundus exam will be conducted.

The indirect ophthalmoscope is adjusted so the light is slightly off center of the examiner's visual field (to reduce glare). The patient's muzzle is held gently and the lens is positioned three to five cm from the cornea and the upper eyelid retracted. The lens is usually held close to the cornea initially to permit observation of the ocular fundus and then moved away from the eye until the image is maximum size. When the hand lens is interposed between the light source and the eye, the fundus is visualized. Image magnification (2X to 4X) is dependent on the dioptric power of the hand lens. The +20 lens is the most versatile. Occasionally, an annoying light reflection occurs and is remedied by slightly tilting the hand lens.

Image magnification is dependent on the dioptric power of the hand lens. The +20 D lens is the most versatile.

The new Welch Allyn Panoptic ophthalmoscope is very nice for learning examination of the retina and optic nerve.

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G. Ultrasonography

Ultrasonography (as in a ship's sonar system) has become increasingly useful in the diagnosis of intraocular disease in the past few years. High frequency sound waves are directed through the eye. A portion of these sound waves "echo" off tissue interfaces. These echoes are amplified and projected onto an oscilloscope. Echoes from the corneal surfaces, the anterior and posterior lens surfaces, the retina, and any abnormal intraocular material will project an image which aids intraocular diagnosis. This is especially useful when dense corneal opacity or mature cataract obscures the view of the fundus.


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.