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CORNEAL DISEASE

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CORNEAL DISEASE

Post  northernwitch on 11/5/2009, 3:27 pm

Corneal Diseases of Dogs and Cats

John S. Sapienza, DVM, Diplomate, American College Of Veterinary Ophthalmologists
Plainview, New York, USA

The cornea is composed of five basic layers: the precorneal tear film, the
epithelium and its basement membrane, the stroma, Descemet's membrane, and the
corneal endothelium.

The transparency of the cornea is based on the lack of blood vessels and cells, the
lack of pigment, the control of corneal water content, and the smooth optical
surface afforded by the precorneal tear film. The cornea can react to disease
in several fashions: with edema, vascularization, scar formation, pigmentation,
cellular infiltration, and the accumulation of abnormal substances.


CORNEAL ULCERS

Corneal ulcers can be divided into superficial and deep stromal ulcers. Superficial
ulcers generally heal quickly and uneventfully. Topical broad-spectrum
antibiotics such as BNP or chloramphenicol QID are advised in addition to
topical atropine TID-QID, as well as a protective Elizabethan collar.

Generally, more aggressive therapy is necessary for deep corneal ulcers, desmetoceles,
iris prolapses, and melting corneal ulcers (keratomalacia). Deep corneal ulcers
(> 1/2 stromal depth) are best treated with surgical intervention; i.e., a
conjunctival pedicle / island graft or a corneal graft. Third eyelid flaps do
not generally provide the support for the weakened cornea.

Corneal lacerations are best to refer to the ophthalmic specialist as early as possible
for prompt repair. If the iris is prolapsed and appears viable, replacement can
be performed or the iris can be amputated if considered necrotic. The cornea is
sutured with 7-0 to 10-0 suture, and the anterior chamber is reformed.

Keratomalacia, or the so-called " melting corneal ulcer, " is common in clinical
practice. Prior to the instillation of any ophthalmic medication, the edge of
the lesion is cultured with a sterile culture swab. Cytology is obtained at the
leading edge of the lesion after the instillation of topical proparacaine.
General guidelines for the appropriate treatment of melting ulcers include:
fortified topical antibiotics (gentamicin, tobramycin, or ciprofloxacin every
1-2 hours), topical serum or plasma, subconjunctival gentamicin or tobramycin,
topical atropine, systemic antibiotics, and often surgery; namely, a
conjunctival graft to provide support, blood vessels and healing serum factors.


Thoughts to Consider

The depth of the ulcer.
Deep ulcers need support in the form of corneal or conjunctival grafts. Third
eyelid flap won't do the job. Deep corneal ulcers rarely improve with topical
medications as the sole therapy. Many deep corneal ulcers proceed to corneal
perforations without the proper surgical intervention and judicious, close
monitoring.

Complicated, infected ulcers need intensive therapy. Initially, I recommend hourly drops!

Anti-collagenase activity needs to be addressed. Topical serum is readily available and
works very well. You must be very aseptic when preparing the patient's serum,
for a sample contaminated with bacteria can iatrogenically super-infect the
lesion. Although many veterinarians commonly use acetylcysteine, experimental
studies show that this product is not very efficacious. Anyway, it smells like
rotten eggs.

Infected corneal ulcers need the " heavy guns " of antibiotics. Fortified solutions can
be made by injecting intravenous antibiotic preparations into the ophthalmicgrade antibiotic bottle.

Atropine is essential for cycloplegia.

Early surgical intervention is important. Many surgical techniques are available in order
to save the globe and to restore good vision.


CORNEAL LESIONS OF THE DOG

Indolent Ulcers
Indolent ulcers are due to a defect in the basement membrane, the corneal
"glue" if you will, which adheres the epithelium to the underlying
corneal stroma. The diagnosis of indolent ulcers is rather straightforward.
With the use of fluorescein stain, one can observe the stain to seemingly
migrate under the edge of the epithelium (the so-called epithelial "
lipping ") due to a detachment of the overlying epithelium to the
underlying stroma. Therapeutic options focus on the re-enforcement or
re-creation of this basement membrane, and to promote the adhesion of the
epithelium to the underlying corneal stroma. Both medical and surgical options
are available. Several topical ophthalmic treatments have been published for
these cases of indolent ulcers and include: topical fibronectin, epithelial
growth factor, serum, polysulfated glycoaminoglycans, aprotinin, and
hyperosmotic agents. Certain ophthalmologists perform a complete superficial
lamellar keratectomy as part of their initial therapy. Other ophthalmologists
use topical ophthalmic grade cyanoacrylate over the debrided corneal bed to
provoke the migration of healing corneal vessels. I prefer to perform, under
topical anesthesia, epithelial debridement and multiple superficial
keratotomies as the initial treatment. After topical debridement and
keratotomies, I place a bandage soft contact lens on the patient's eye, and
administer topical triple antibiotic solution and atropine solution. One must
be very careful not to create too deep a keratotomy to the eye. Furthermore,
keratotomies are contraindicated in cats with indolent ulcers, for the
keratotomies may predispose the cat to the formation of a corneal sequestrum
(focal corneal necrosis). An Elizabethan collar is always advised to minimize
self-trauma to the eye. Ointments are not recommended, as they may inhibit
corneal healing. Likewise, topical aminoglycosides (namely, gentamicin) are not
advised due to their epitheliotoxicity. Indolent ulcers take usually 2-4 weeks
to heal. In certain cases of indolent ulcers, especially in Boxers, the dogs
heal with excessive vascularization to even frank granulation tissue formation.
When the ulcer is healed, as evidenced by no fluorescein retention, a topical
lubricant ointment is applied to improve the regularity and smoothness of the
cornea. Topical corticosteroids are never prescribed by me to improve the
vascularization. I prefer to allow time to heal the cornea, rather than risk
another episode of corneal ulceration.

Keratoconjunctivitis Sicca: Dry Eye Syndrome

Keratoconjunctivitis sicca, or KCS, is one of the most frequent causes of corneal disease in the
dog. Whenever one observes a canine patient with a mucoid or mucopurulent
ocular discharge, dry-appearing cornea, or corneal pigmentation, the diagnosis
of KCS must be entertained. Although less frequently diagnosed in the feline
species, KCS does indeed affect the cat and is most commonly associated with
herpesvirus infection (past or present). The clinical signs of KCS are varied,
and can include a mucoid to mucopurulent ocular discharge, conjunctivitis,
keratitis, dull-appearing cornea ("lack-luster cornea "), pigmentary
keratitis, acute-forming corneal ulcers (even corneal ruptures with an iris
prolapse), and blindness. The majority of causes of KCS in dogs are considered
to be idiopathic, with an immune-mediated basis. KCS may or may not be
associated with concurrent systemic illnesses such as diabetes mellitus, lupus,
and hypothyroidism, A minority of KCS cases can be attributed to a specific
cause such as secondary to canine distemper virus infection, idiosyncratic
reaction to oral sulfonamides, reactions to other drugs, i.e., topical atropine
or anesthetics (proparacaine, lidocaine, tetracaine), and recently noted
secondary to etodolac (EtoGesic®), congenital hypoplasia or aplasia of the
lacrimal glands, facial neuropathy, and removal of the third eyelid gland. Do not
even think of removing the third eyelid gland in these cherry eye cases!!!

The diagnosis of KCS is relatively straightforward. A Schirmer tear test (STT) is
left in the lower conjunctival fornix for one minute, and a reading of > 10
mm wetting per minute is considered normal, between 6-10 mm as suspicious for
KCS, and <5 mm as diagnostic for dry eye. Rose Bengal staining of the eye
can demonstrate early corneal or conjunctival lesions. Diffuse pigmentary
keratitis may be seen in very chronic cases of KCS. NOTE: Do a STT on
all cases of red eyes with a mucoid / mucopurulent ocular discharge.


The goals of KCS therapy are three-fold:
To substitute tears.

To stimulate tear production.

To treat any underlyinginfection.

Artificial tears (Refresh®, Celluvisc®, Hylashield®) can be used to substitute tears, but
literally must be instilled every 30-60 minutes if used as sole therapy for dry
eyes. This not only is impractical, but also not necessary for our patients.
Use artificial tears as adjunctive therapy for KCS, not as the only therapeutic
option for tear replacement.

Stimulation of tear production can be achieved by the use of pilocarpine (oral or topical
therapy) and topical cyclosporine A therapy. A dilute (1/4 %) pilocarpine
solution can be used as a topical drop or oral 2 % pilocarpine can be added to
the food

(At 1 drop of a 2 % pilocarpine solution per 10 kg. body weight). Cyclosporine A
(CSA) is the treatment of choice for KCS. One can use topical CSA every 12
hours as a 1-2 % solution (mixed in corn or mineral oil) or the commercially
prepared 0.2 % ointment (Optimmune®). I find that the topical solution to be
very effective, easier for clients to instill, and cheaper in long-term usage
compared to the ointment preparation. If the STT is greater than 4 mm wetting
per minute, there is a 80-85% chance for improvement with cyclosporine therapy.
If the initial STT is less than 2 mm wetting per minute, there is a 60-65%
improvement in tear production after starting CSA therapy. Topical antibiotics
are prescribed to control and to prevent local ocular infections.
Broad-spectrum antibiotics are recommended twice daily.


KCS is a controlled, often not curable syndrome. Therapy usually is for life! For cases
refractory to topical and oral therapies, a parotid duct transposition can be
considered. This surgery replaces the dry eye with salivary secretions.
Although saliva does not have the exact composition as tears, saliva is a very
good substitute in most cases of dry eyes. Complications of a parotid duct
transposition include: the risk of anesthesia, salivary precipitates unto the
eye, excessive facial wetting, and stenosis of the parotid duct.

Pannus

The term pannus, or nowadays more appropriately named, chronic superficial keratitis
(or CSK)
literally denotes corneal pigmentation and vascularization. Pannus
or CSK is a commonly diagnosed corneal disorder that we observe most frequently
in the German Shepherd Dog. Other breeds affected with CSK include the
Greyhound, Siberian Husky, Belgian Shepherd, Poodle, and Miniature Pincher.

The cause of CSK is unknown, but we consider it to be an immune-mediated disease whereby
corneal antigens have been altered, and an autoimmune reaction is occurring.
Ultraviolet radiation and elevation have additive effects in the severity of
this disorder. Furthermore, young affected dogs seem to have a more aggressive
and unforgiving corneal disease. The clinical signs seen with CSK are the
classical pigmentation and vascularization, typically occurring at the lateral
aspect of the cornea. With time, the lesion will progress to cover the entire
cornea. An atypical form of CSK is seen where the third eyelid is solely
affected, and we call this condition "atypical pannus" or
"plasmoma." Both corneal and third eyelid diseases can occur at the
same time. The diagnosis of CSK or pannus is straightforward. The typical
corneal lesions affecting the lateral aspect of the cornea in a German Shepherd
( or other predisposed breed ) are evidence enough for the diagnosis of pannus.
Cytology can be obtained from either a corneal or third eyelid scraping to
yield lymphocytes or plasma cells. Diagnosis, however, is usually made on a
clinical basis. Treatment for CSK is varied depending upon the extent of the
lesions. Remember that a markedly pigmented cornea will be more difficult to
treat than an earlier lesion of mild corneal pigmentation and vascularization.
Also, young affected dogs are more resistant to therapy. Equally important to
therapy is the education of your client that CSK is a life-long disease without
cure! We are trying to control the disease, but a cure is never obtained. The
mainstay of therapy is topical steroids. I prefer to use either topical
dexamethasone or prednisolone acetate TID-QID. In addition to topical steroids,
I frequently add topical cyclosporine therapy (2 % drops or Optimmune® ointment
BID). Subconjunctival steroids can be administered for severe corneal lesions,
but I prefer not to give subconjunctival injections unless all other avenues of
therapy have been first exhausted. Once you give a subconjunctival injection,
you are committed to one month of reposital corticosteroid therapy!!!
Cryosurgery has been used by some, but I would not advocate its common practice
for pannus. Superficial keratectomy can be performed to remove advanced corneal
pigmentation, but one is limited to 2-3 keratectomies per eye, and topical
corticosteroid therapy will have to be used soon after surgery to halt the next
"wave" of advancing corneal pannus. Beta-irradiation with a Strontium
90 probe is an excellent choice for advanced pannus, but these probes are
available at university settings. Pannus or chronic superficial keratitis is a
common corneal disease that requires lifetime therapy. Control of ocular signs
is the goal with cures not possible.

Corneal Dystrophy and Degeneration

The term Corneal Dystrophy is best used for a corneal opacity which is bilateral and
symmetrical in presentation, has a familial basis, is not associated with
inflammation, is not progressive (or minimally progressive), and is not
associated with a systemic disorder. Corneal dystrophies typically involve the
superficial epithelial or anterior stromal layer of the cornea, but there also
exists a subcategory of dystrophies, which involve the corneal endothelium,
causing bilateral, diffuse corneal edema. The superficial corneal dystrophies
are commonly seen in the Siberian Husky, Bichon Frise, American Cocker Spaniel,
Collie, German Shepherd, Shetland Sheepdog, and Cavalier King Charles Spaniel.
The endothelial corneal dystrophies most commonly are observed in the
Chihuahua, Boston Terrier, and the Dachshund. The superficial corneal lesions
rarely need therapy, for the animals usually are not symptomatic. The
endothelial dystrophies frequently result in diffuse corneal edema and the
formation of bullae (bullous keratopathy). Topical hyperosmotic agents (such as
5% NaCl ointment) can be used with variable results. Thermal keratoplasties can
be performed whereby the superficial aspect of the cornea is delicately
cauterized with a special low-temperature ophthalmic cautery unit. Penetrating
keratoplasty (or a corneal transplant) can be attempted in the very advanced
cases of blinding corneal edema.

In contrast to corneal dystrophy, Corneal Degeneration occurs secondary to
pathologic changes within the cornea. Lipid, cholesterol, calcium or a
combination thereof are often deposited in the lesion. Corneal degenerations
are unilateral or bilaterally asymmetrical, often associated with inflammation
(vascularization and / or pigmentation), and may be associated with a systemic
disorder (such as hypothyroidism, Cushing's disease or metabolic derangements
of cholesterol or triglyceride metabolism). Therapy for corneal degeneration
depends upon the extent of the lesion. Several therapies include the following:
topical ophthalmic lubricants (to improve the tear film), cyclosporine (to
improve the tear film and to provide immunomodulatory function), calcium
binders such as EDTA (to bind to the calcific material), and topical
antibiotics (to prevent against infection). Surgical options include a
superficial keratectomy (to remove the degenerative material), conjunctival
grafts (to provide support), excimer laser ablation of the lesions, corneal
cyanoacrylate application, and donor corneal transplants.

Episcleritis Or Nodular Granulomatous Episcleritis

Episcleritis, or the inflammation of the tissue underlying the conjunctiva and overlying the
sclera, can present to the clinician in several fashions. We can observe a
focal elevation of the scleral-episcleral-conjunctival tissue especially near
the limbus. This focal elevation can present as a tumor-like growth.
Many times, we will call this a focal episcleritis or a nodular granulomatous
episcleritis (NGE). In addition, we can see a diffuse infiltration of
the episcleral tissue, emanating around the limbus in one or both eyes.
Episcleritis often is a clinical diagnosis, but ultimately biopsy of the
affected lesion is the definitive diagnosis. Histopathologic features of
episcleritis are consistent with those of chronic granulomatous inflammation.
Differential diagnosis for episcleritis and NGE-like lesions include:
neoplasia, excessive granulation tissue, cysts, foreign body, focal infections,
granulomas, and uveitis to name a few. Breeds predisposed to episcleritis
include the Collie, Shetland Sheepdog, Cocker Spaniel, Rottweiler, and Labrador
Retriever. Therapeutic options for episcleritis are multiple, and include:
surgical debulking with adjunctive cryotherapy, beta-irradiation, intralesional
corticosteroid injections, topical steroid therapy, topical cyclosporine
solution, oral corticosteroid, azathioprine and the combination of tetracycline
and niacinamide administration. For initial therapy, I like to obtain a biopsy
of the affected lesion to confirm the diagnosis and then to perform cryotherapy
of the surgical site. If the owners are reluctant to perform surgery or if the
patient is a poor anesthetic candidate, topical or oral medications can be
attempted. Frequently, I will give an intralesional injection of betamethasone
or triamcinolone, as well as to administer topical corticosteroid drops
(dexamethasone or prednisolone acetate). If the dog responds favorably to
therapy, the treatment regime is tapered to daily or every other day frequency.
If the animal does not respond to topical medications or if the patient is
difficult to treat with topical solutions, then oral immunosuppressive therapy
can be attempted. Oral prednisone can be prescribed, but I find that oral
azathioprine (1-2.0mg/kg once daily for 3 days, then 0.75 to 1.0 mg/kg every 3
to 7 days) is an excellent therapeutic option in many cases of episcleritis.
Toxic side effects with azathioprine include: vomiting, diarrhea,
hepatotoxicosis, and myelosuppression. Recently, some ophthalmologists have
reported success with oral administration of the combination of tetracycline
and niacinamide for episcleritis in dogs. My experience with this combination
of medications has been less than satisfactory. In addition, oral interferon
(Roferon-A®, 80 IU/dog/day) has been found to be quite successful in cases of
idiopathic ocular granulomatous diseases in collies (R.C. Riis, Abstract,
Annual ACVO meeting, Montreal, 2000).


Corneal Neoplasia

Corneal neoplasia is rare, and many times actually arise from the limbal region. Examples
of corneal tumors include adenocarcinoma, papilloma, fibrosarcoma, hemangioma,
hemangiosarcoma, limbal melanoma, and corneal lymphosarcoma. Prognosis will
depend on tumor type, infiltration, and associated ocular abnormalities.


UNIQUE CORNEAL LESIONS OF THE CAT

Herpesvirus

Feline herpesvirus is caused by feline rhinotracheitis virus-1 (FHV-1). A wide
spectrum of clinical syndromes may be observed in the feline herpes patient.
Herpesvirus commonly causes keratitis, and may also contribute to the formation
of conjunctivitis, as well. In fact, the scenario of keratitis in the face of
an associated conjunctivitis is almost always due to feline herpesvirus. In
kittens, FHV-1 is one of the agents responsible for the neonatal ophthalmia
syndrome, whereby an infection is observed under the closed eyelids.
Herpesvirus frequently causes corneal ulceration, which can present as punctate
keratitis, dendritic ulcers (looks like a dendrite of an axon), geographic
keratitis (large corneal infections and ulcers), and stromal keratitis (often
due to an immune reaction to altered viral or corneal antigens). Diagnosis is
based on clinical presentation (keratitis / conjunctivitis, symblepharon,
eosinophilic conjunctivitis, etc), the presence of intranuclear inclusion bodies
on cytology, pathognomic lesions such as dendritic ulcers, and laboratory
testing which include immunofluorescence (IFA frequently results in false
negative results) and polymerase chain reaction (PCR). At this time, PCR is
considered the most sensitive test for FHV-1. However, available PCR testing
has been less than satisfactory from available clinical laboratories. Therapy
for FHV-1 include the use of topical antiviral agents such as trifluridine
(Viroptic®), idoxuridine (obtained from a compounding pharmacy), and adenine
arabinoside (Vira-A®) for a minimum of 4-6 times daily initially for the first
week, oral L-lysine (250-500 mg orally BID mixed in the food), and other agents
such as oral or topical interferon, acyclovir (50 mg every 12 hours for no more
than 14 days), and famcyclovir (125 mg: ¼ tablet orally twice daily for 8
days). Treatment with topical antiviral medications and oral L-lysine can last
for months at a tapered dose. The prognosis for FHV-1 infection is generally
fair to good, but always warn owners of the necessary long-term therapy and
potential for frequent recurrences. Several sequelae to FHV-1 infection in cats
include corneal sequestrum formation, symblepharon (the adhesion of conjunctiva
to conjunctiva or to the cornea), dry eye formation (KCS), and the presence of
eosinophilic conjunctivitis or eosinophilic keratitis.


Corneal Sequestrum Formation

Corneal sequestrum formation is a unique condition to the feline eye (also has recently
been described in the equine eye). Also known as corneal nigrum, corneal
mummification, and corneal necrosis, sequestrum formation can result from any
condition leading to chronic corneal irritation. Examples include feline
herpesvirus infection, entropion, distichiasis, exposure keratitis, trauma, KCS,
lagophthalmos, and genetic predisposition as seen in the Persian and Himalayan
breed. There are two main thoughts for treatment of corneal sequestrum
formation with those treating the eyes topically with ophthalmic preparations
until the sequestrum sloughs off, and those who surgically remove the
sequestrum with a keratectomy and corneal grafting techniques. Because I have
observed several cats with corneal sequestra, which have perforated when
allowed to slough off on their own, rather to surgically remove the lesion, I
prefer to remove the sequestrum with a keratectomy and then to perform a
corneoconjunctival transposition or conjunctival graft procedure.


Eosinophilic Keratitis
Eosinophilic keratitis is another unique ocular syndrome to the cat (also seen in equine
patients), which is readily diagnosed with a corneal scraping and cytology or a
corneal biopsy (not necessary in most cases). The corneal cytology demonstrates
an infiltration of eosinophils, mast cells or a combination of the two cell
types. Single to multiple progressive lesions are observed to originate from
the limbus (often at the lateral aspect of the eye, but can be seen as a medial
lesion, as well). Treatment for eosinophilic keratitis includes topical and
systemic anti-inflammatory agents. Topical dexamethasone or prednisolone are
effective to control the lesion, as well as oral megestrol acetate (Ovaban®).
The author tends not to use the above medications for concern to recrudesce a
latent herpesvirus infection or for the secondary side effects seen with
megestrol acetate. I prefer to use topical cyclosporine (1.5% to 2%) solution
two to three times daily as initial therapy. Control, not cure, of the lesion
is the ultimate goal.

References

1. Glaze MB, Gelatt KN. Feline Ophthalmology. In: Veterinary Ophthalmology. Third
edition ( ed. Gelatt KN ), Lippincott Williams & Wilkins, Philadelphia.
1999:997-1052.

2. Nasisse MP, Weigler BJ. The Diagnosis of Ocular Feline Herpesvirus Infection. Vet Comp
Ophthalmol 1997: 7: 44.

3. Nasisse MP. Manifestations, diagnosis, and treatment of ocular herpesvirus infection in
the cat. Comp Cont Educ Pract Vet 1982:4:962.

4. Champagne E, Munger R. Multiple punctate keratotomy for the treatment of recurrent
epithelial erosions in dogs. J Am Anim Hosp Assoc 1992; 28: 213-216.

5. Gelatt K, Samuelson D. Recurrent corneal erosions and epithelial dystrophy in the
boxer dog. J Am Anim Hosp Assoc 1982; 18: 453-460.

6. Kirschner SE. Persistent corneal ulcers. What to do when ulcers won't heal. Vet Clin
North Am Small Anim Pract 1990; 20:627-642.

7. Kirschner SE, Brazzell RK, Stern ME, et al. The use of topical epidermal growth factor
for the treatment of nonhealing corneal erosions in dogs. J Am Anim Hosp Assoc
1991; 27-449-452.

8. Miller W. Using polysulfated glycoaminoglycans to treat persistent corneal erosions in
dogs. Vet Med 1996; 71: 916-922.

9. Gelatt KN: Essential of Veterinary Ophthalmology. Lippincott Williams & Wilkins,
Philadelphia. 2000: 125-164..

10. Slatter D. Fundamentals of Veterinary Ophthalmology, Vol 1, 2nd. Edition. WB Saunders
Co. Philadelphia, 1990:257-303.

11. RD Whitley, GilgerBC. Diseases of Canine Cornea and Sclera. In: Veterinary
Ophthalmology. Third edition ( ed. Gelatt KN ), Lippincott Williams &
Wilkins, Philadelphia. 1999:635-673.

12. Gilger BC, Whitley RD. Surgery of the Cornea and Sclera. In: Veterinary Ophthalmology.
Third edition ( ed. Gelatt KN ), Lippincott Williams & Wilkins,
Philadelphia. 1999:675-700.

Speaker

John S. Sapienza, DVM, Diplomate
American College Of Veterinary Ophthalmologists
Plainview, New York, USA

Dum degree - 1987 Cornell
University

Internship
- Animal Medical Center

Residency
in Comparative Ophthalmology - University of Florida

Diplomate,
AWO 1993

Staff
Ophalmologist, Long Island Veterinary Specialist

Consultant:
New York Aquarium, Atlantis Aquarium, Bronx Zoo


Last edited by northernwitch on 11/5/2009, 6:16 pm; edited 1 time in total
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Re: CORNEAL DISEASE

Post  Pugsaunt on 11/5/2009, 3:47 pm

Thank you, Blanche. I thought I knew a bit about eye problems, and this article was a whole new education.
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Re: CORNEAL DISEASE

Post  akc0104 on 11/5/2009, 5:57 pm

Thanks Blanche! My Bob is going to take me down a whole new path of eye issues and that was a great primer for our appt on Tuesday.
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Re: CORNEAL DISEASE

Post  leslyeb on 11/6/2009, 8:53 am

Lisa.
If Bob might have eye problems, do you know about the eye specialist on Nolensville Rd?



akc0104 wrote:Thanks Blanche! My Bob is going to take me down a whole new path of eye issues and that was a great primer for our appt on Tuesday.
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Re: CORNEAL DISEASE

Post  akc0104 on 11/6/2009, 10:29 am

leslyeb wrote:Lisa.
If Bob might have eye problems, do you know about the eye specialist on Nolensville Rd?



akc0104 wrote:Thanks Blanche! My Bob is going to take me down a whole new path of eye issues and that was a great primer for our appt on Tuesday.

Yes. We have an appointment with Dr Laratta in Nolensville on Tuesday afternoon.
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Re: CORNEAL DISEASE

Post  leslyeb on 11/6/2009, 1:20 pm

I have only seen the female doctor there whos name I can't remember at the moment. I hope the appointment goes well. Do you have any idea what problems he may have? Are his eyes dry?



akc0104 wrote:
leslyeb wrote:Lisa.
If Bob might have eye problems, do you know about the eye specialist on Nolensville Rd?



akc0104 wrote:Thanks Blanche! My Bob is going to take me down a whole new path of eye issues and that was a great primer for our appt on Tuesday.

Yes. We have an appointment with Dr Laratta in Nolensville on Tuesday afternoon.
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Re: CORNEAL DISEASE

Post  akc0104 on 11/6/2009, 1:26 pm

No, they're not dry. He has pigmentary keratitis in his right eye and several small ulcers in the same eye. My vet wasn't sure that he could see out of that eye at all, she felt it is really advanced for a puppy his age. I've been doing ointment this week to help with the ulcers and then we'll go in on Tuesday.
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