Ocular Manifestations of Systemic Diseases in Small Animals |
By Dennis E. Brooks, DVM, PhD, Diplomate ACVO |
INTRODUCTION
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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BACTERIA INFECTIONS
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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CANINE DISTEMPER VIRUS

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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INFECTIOUS CANINE HEPATITIS
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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FELINE HERPES VIRUS (RHINOTRACHEITIS)
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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FELINE INFECTIOUS PERITONITIS (FIP)
causes uveitis and chorioretinitis
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FELINE LEUKEMIA VIRUS
causes uveitis and chorioretinitis
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TOXOPLASMOSIS
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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FUNGAL DISEASES
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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EHRLICHIA CANIS
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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CHLAMYDIA PSITTACI
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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MISCELLANEOUS SYSTEMIC DISEASES
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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HYPERVISCOSITY SYNDROME
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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ARTERIAL HYPERTENSION
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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HORNER'S SYNDROME
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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CANINE UVEODERMATOLOGICAL SYNDROME (VKH-LIKE)
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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RETICULOSIS OR GRANULOMATOUS MENINGOENCEPHALITIS (GME)
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
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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DIABETES MELLITUS
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
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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EXTRAOCULAR MUSCLE MYOSITIS
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
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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EYELID NEOPLASMS
The majority of canine eyelid tumors are benign. Those that appear
histologically malignant tend to be infiltrative but rarely metastasize.
- 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.
- 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.
- 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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EYELASH DISEASES
Distichiasis/Districhiasis
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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KERATOCONJUNCTIVITIS SICCA (KCS)
Aqueous deficiency of the precorneal tear film (PTF)
causing progressive inflammatory changes of the cornea and conjunctiva.
Diagnosis
- Clinical signs
- Schirmer tear test: Normal 15-25 mm/minute; Suspicious = 8-10 mm/minute;
Low = <8 mm/minute
- Rose bengal stain - epithelium of conjunctiva and cornea will remain red if
devitalized or necrotic.
- 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).
Incidence
Breeds at Risk - English Bulldog , West Highland
White Terrier, Lhasa Apso, Pug, Cocker Spaniel, Pekingese, Yorkshire
Terrier, Shih Tzu, Miniature Schnauzer, Boston Terrier
Etiology
- Congenital/inherited: Pug, Yorkshire Terrier, Miniature Schnauzer,
American Cocker Spaniel, English Bulldog, Beagle
- Drug related:
- Atropine: Topical and systemic
- Sulfonamides: sulfadiazine, salicylazosulfapyridine (Azulfidine®),
Tribrissin®- small dogs at increased risk
- Systemic diseases: Canine distemper virus
- Chronic blepharoconjunctivitis - scarring of lacrimal ducts
- Neurogenic
- Other "associated" diseases: **Immune related disorder suspected in up to
40% of cases. Hypothyroidism, Hyperadrenocorticism, Diabetes mellitus, Demodectic
mange, SLE, RA
- Trauma to the orbit and lacrimal gland
- 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.
Treatment
Medical
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:
- Replace tears - Hypotears (CIBA Vision); Tears Naturale (Alcon); Lacrilube
(Allergen); Duratears (Alcon); Lacriserts (Merck)
- Stimulate production of tears
Topical 0.2% Cyclosporine (OPTIMUNE): DRUG OF CHOICE FOR KCS, BID
Topical 0.03% Tacrolimus BID for CSA nonresponders.
- Control bacterial flora - topical broad spectrum antibiotic BID, eg. triple
antibiotic or chloramphenicol ointment
- Control inflammation - topical corticosteroids, may combine with topical
antibiotic (TriOptic-S, triple antibiotic with hydrocortisone); USE ONLY IF NO
CORNEAL ULCERATION!!
Surgical therapy
- Conjunctival flap - Deep corneal ulcers, to provide corrective tissue and blood vessels.
- 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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LACRIMAL SYSTEM DISEASE
Outflow System: Most common clinical sign is epiphora.
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IMPERFORATE PUNCTA OR PUNCTAL MEMBRANES
American Cocker Spaniel, Toy and Miniature Poodle
Obstructions of Nasolacrimal System
Etiology:
- Congenital absence of inferior canaliculus
- Inflammatory = dacryocystitis
- Foreign body
- Secondary to scarring - traumatic, inflammatory
Signs - Depends on cause:
- Inflammatory/foreign body/neoplastic
- epiphora - mucopurulent discharge
- conjunctivitis
- pain on palpation of medial canthus region
- abscessation in severe cases
- Congenital/scarring/neoplastic
- epiphora
Diagnosis
- Negative fluorescein passage
- Flushing duct to recover material
- Dacryocystorhinography
Treatment:
- Infectiona and Anti-Inflammatory
- Systemic antibiotics and corticosteroids
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CONJUNCTIVA
THE EYE GETS RED OR HAS CONJUNCTIVITIS IN NEARLY ALL
TYPES OF EYE DISEASE. THE EYE HAS LIMITED WAYS TO REACT TO INJURY!
Conjunctivitis
Most common extraocular problem in practice
Diagnostic tests for conjunctivitis
- STT and PRT- routine on all conjunctivitis cases
- Culture/sensitivity - fornix, not routinely done
- Cytology - topical anesthetic, spatula
- IFA and PCR tests for herpes and chlamydia in cats
Etiologies of conjunctivitis
- Bacterial conjunctivitis = purulent discharge
- Viral conjunctivitis - frequently bilateral, may be unilateral
- Allergic conjunctivitis - frequent cause
- Physical irritation conjunctivitis - wind, dust, foreign bodies, eyelid
disease, etc.; frequent cause
- Keratoconjunctivitis sicca conjunctivitis
Nictitating Membrane - Eversion of Cartilage
- Cartilage is abnormally formed, causes nictitans to roll inward or outward. Seen
in Basset Hounds and Weimaraners.
- Decreased function, cosmetically unacceptable. Can lead to chronic irritation.
Can be associated with "cherry eyes".
- Treatment = surgical removal of affected cartilage
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Hypertrophy and prolapse of nictitans gland (CHERRY EYE)
- Primarily seen in young dogs, less than 2 years
- Most common in Beagles, American Cocker Spaniels, Pekingese
- Gland protrudes above free border of the TE, becomes inflamed and enlarged.
May see epiphora, mucoid discharge and conjunctival inflammation.
- Treatment
- Medical - physically replace gland, topical corticosteroids - frequently recurs.
- 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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