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EYE PROBLEMS IN DOGS
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GLAUCOMA
Glaucoma is defined as excessive pressure inside the eye. The
eye is full of a fluid called the aqueous humor, which is constantly
produced and drained away from the eye and supplies nutrition for all
interior
structures. Glaucoma is caused by a decrease in the amount of fluid
that
flows out of the eye. It is a serious disease and without proper
treatment
can result in blindness. Unfortunately, even with aggressive medical
and surgical therapy, dogs and cats with glaucoma will often lose their
vision. Glaucoma is one of the most frequent causes of blindness in
adult
dogs.
Types of Glaucoma:
There are two main types of glaucoma, primary and secondary. In primary
glaucoma, the cause of the increase in pressure is due to decreased
outflow from the drainage angle. It is frequently an inherited problem.
Beagles, Basset Hounds, and Cocker Spaniels are especially prone to
this type of glaucoma. In secondary glaucoma the pressure is too high
because something else is wrong in the eye, such as a lens luxation,
bleeding, inflammation, or tumor.
Aqueous humor made in the ciliary body flows through the pupil into the
anterior chamber. Aqueous then drains into the bloodstream through the
iridocorneal angle.
Signs of Glaucoma:
1. A red (bloodshot) eye
2. A painful eye
3. Lids may be held shut
4. Excessive tearing
5. Eye may appear cloudy or blue
6. Sudden blindness
7. A dilated (enlarged) pupil that does not respond normally to light
8. Depression
9. Appetite loss
10. Enlargement of the eye
Treatment:
The treatment chosen (i.e. surgery and/or medical therapy) will be
influenced by what the goal of therapy is: to stop pain in a blind eye
or to preserve vision. Medical treatment consists of a number of
different drugs used in combination. Some are given by mouth and effect
the whole body, while others are put directly into the eye and have a
local effect. The drugs that work when the problem is first diagnosed
may not work forever. Therefore, the intraocular pressure needs to be
monitored on a regular
basis so that the medication regimen can be altered to fit the needs of
the patient. Unfortunately glaucoma cannot be cured, only controlled.
When medical treatment fails, surgical therapy can help prolong vision,
or eliminate pain.
Medical Therapy:
The following categories of drugs are frequently used:
Carbonic anhydrase inhibitors: Oral and topical formulations
reduce the amount of fluid produced inside the eye. (Methazolamide,
dorzolamide or Trusopt )
Miotics (Parasympathomimetics): Used on the eye, they help to
increase the outflow of fluid from the eye. They may cause a temporary
redness, burning or stinging in the eye. (Pilocarpine)
Beta-adrenergic blockers: reduces the amount of fluid produced
inside the eye. (Timolol)
*By using very small amounts of several of the drugs, the risks of side
effects can be reduced.
*Please keep these drugs out of the reach of
children.
Surgical Treatment:
In some cases, surgical procedures are available that may help to
provide long-term control. One of these procedures uses a laser to
destroy the part of the eye that produces fluid and thereby reduces the
pressure. Another surgery inserts a tube into the eye that shunts the
fluid under the conjunctiva (pink tissue) deep in the eye socket.
Neither surgery is 100% effective and multiple surgeries over several
years may be required to preserve vision.
A blind, painful eye can be removed to eliminate discomfort for your
pet and to avoid the need for medicines that are expensive and affect
the whole body. The surgery to remove the eye is called enucleation.
After the eye is removed, the eyelids are permanently sewn shut. This
means that the dog will look like he or she is winking at you.
Blind painful eyes may also have an intraocular prosthesis placed after
a procedure called evisceration. With this surgery the contents of
the eye are removed and silicone prosthesis is placed inside the eye.
The
outward appearance of the eye is preserved but no longer has the pain
from
high pressure. Afterwards, the eye looks fairly normal, but remains
blind.
EVISCERATION WITH PLACEMENT OF AN INTRASCLERAL PROSTHESIS
This surgical procedure is a cosmetic alternative to enucleation
and is performed on blind and painful eyes. The contents of the eye are
removed and a sterile silicone ball (the prosthesis) is placed within
the eye. The looks fairly normal, moves normally, remains blind, but is
no longer a source of pain. The photographs below show a dog with
prostheses
in both eyes (the smaller photo is a closer view.
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Remember:
Each case is different and therapy must be tailored to the individual
patient. Intraocular pressure must be measured regularly and the eye
should be treated as prescribed. Do not stop any medication unless
directed to do so by your veterinarian.
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KERATOCONJUNCTIVITIS SICCA (DRY EYE)
Keratoconjunctivitis sicca (KCS) is also called dry eye. This condition
is due to a deficiency in tear production and results in a red, itchy
eye with a thick mucous discharge. The tear production is measured by
the
Schirmer Tear Test. In this test a standardized paper strip is gently
placed
on the eye and allowed to absorb tears for one minute. Wetting values
of
less than 15 mm per minute are abnormal.
DRY EYE: Below are two dogs with dry eye.
The cornea is the front window of the eye. In the normal eye it is kept
clear, moist, and smooth, by the tear film. In the condition of dry
eye, the cornea is vulnerable to exposure, dry air, and bacteria. In
order to protect itself, scar tissue starts to cover the normally clear
cornea. This tissue consists of blood vessels, and pigment and results
in a thickening of the cornea so that it appears dull and cloudy (photo
on the left below). Tears are made of mucus, water and oils. Dry eye is
a deficiency of the watery (or aqueous) part of the tears. Therefore,
animals with KCS, accumulate a lot of mucus (photo on the right).
Why does this happen?
Acute KCS results in a very red and painful eye with a lot of
discharge. The condition may be associated with viral diseases, trauma,
drug toxicity (some types of antibiotics and some types of
non-steroidal anti-inflammatory medications for example), allergy, or
general anesthesia.
Chronic KCS results in intermittent redness with a profuse, ropy, thick
discharge that adheres to the eye. Without treatment, the cornea may
eventually pigment and scar to result in loss of vision. This can be
familial in certain breeds, associated with immune-mediated diseases,
secondary
to chronic inflammation of the eye, or idiopathic (no known cause).
How long will this problem last?
Sometimes the condition resolves and spontaneous tear production
resumes. The acute form is more likely to resolve. Chronic KCS may or
may not resolve, and those animals with lower tear values (near zero)
are harder to control. Medical therapy may need to be given for the
lifetime
of the animal. If medical therapy fails, surgery to transplant a
salivary
gland duct into the eye can sometimes help control the problem.
The importance of reexamination:
The tear test should be repeated to monitor progress and improvement in
tear production. Premature discontinuation of the treatment can allow
the condition to worsen. Due to corneal pigmentation and scarring, the
condition can cause blindness if left untreated.
How is this treated?
Animals with acute dry eye frequently have corneal ulcers and they must
be treated aggressively with antibiotics and tear replacement to
avoid perforation and loss of the eye. Both acute and chronic KCS are
treated by topical tear substitutes as well as stimulation of existing
tear production. Cyclosporine ointment (Optimmune , Schering Plough) is
used to increase tear production and reduce inflammation. Sometimes
cyclosporine
used 2x/day can control the KCS effectively without additional
medications.
In some cases, topical antibiotics and/or corticosteroids are used in
the treatment of KCS. The tear film has natural antibacterial action
that must be replaced by antibiotic therapy. Anti-inflammatory drugs
are frequently used to help control scarring and irritation.
It is important to clean accumulated mucus from eyes or lids with eye
wash and cotton balls prior to instilling medications.
Be sure to keep all medications out of the
reach of children.
Follow the medication schedule that you have been given. Premature
discontinuation of medication is the most common cause of treatment
failure.
Important Note:
If your pet is on a topical steroid (hydrocortisone, dexamethasone, or
prednisolone), always call your veterinarian if your pet exhibits signs
of pain (squinting, or rubbing at the eye). If a corneal ulcer
develops, topical steroids must be discontinued immediately. When in
doubt, stop
topical steroids until your veterinarian checks the eye.
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CORNEAL ULCERATION
The cornea is the front clear part of the eye and is covered with a
clear epithelium (skin layer). The corneal epithelium is like our skin
except that it is clear and smoother. If the corneal epithelium is
scratched, scraped or rubbed off, the resulting defect is called a
corneal ulcer. This
condition is painful and animals with ulcers often squint and rub at
their
eyes.
A corneal ulcer can be a sight-threatening emergency if it deepens or
becomes infected. This can happen rapidly (overnight), so prompt
attention to a painful eye is essential.
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PROGRESSIVE RETINAL ATROPHY (PRA)
Progressive retinal atrophy (PRA) is a name given to a group of eye
diseases of similar character. PRA causes no pain or discomfort but may
result in permanent blindness. The word atrophy means wasting away.
PRA develops after birth and in some breeds has been determined
to be inherited from both parents. It affects the retina, which lines
the back portion of the inside of the eye. The retina contains the
light-sensitive rods and cones that change light into energy for
transmitting messages to the brain. The retina is similar to the film
in a camera; the image or
picture is received on it.
PRA can occur in all breeds of dogs and cats although certain
breeds are at higher risk. It appears earlier in some breeds and can
take several years to cause complete blindness. An early sign of PRA is
inability to see in dim light or at night. For example, an animal with
PRA may hesitate to go from a well-lighted room into a darkened room.
Due to PRA's slow progress, most pets adapt very well to the gradual
loss of sight. Many owners do not realize their pet is becoming blind.
Animals compensate well for blindness, because their senses are much
more acute than those of people
Important Points
about PRA:
- No effective treatment
is available.
2.
Complete blindness
eventually
results.
3. The condition, however, is not painful
4. PRA is prevented through selective breeding of
animals with normal eyes.
5. Sometimes cataracts develop secondary to the
retinal degeneration. But because of the retinal
degeneration, cataract removal would not help the animal regain
vision.
6. Poor vision in dim light is the first sign you
will see in your dog.
7. You may also eventually see dilated pupils.
Notify the Vet if Any of the Following Occur
You
notice a sudden change in your pet's vision or in the appearance of the
eyes.
Your pet shows
pain or discomfort.
CATARACTS
A cataract is opacity of the lens of the eye. The lens is behind
the iris (the brown or blue part of the eye) and can change its shape
allowing animals to see close objects. A thin capsule (the consistency
of cellophane) covers the lens.
In front of the lens is a clear fluid, called aqueous humor, and
behind the lens is a clear gel, called the vitreous humor. The vitreous
helps keep the retina attached. The retina is a layer of cells that
functions in a manner similar to the film in a camera; it receives
light and allows animals to see.
Causes of Cataracts
Cataracts may develop because of an inherited defect, with age, or
secondary to inflammation, trauma, diabetes, or retinal degeneration.
Cataract Progression
As cataracts progress, they go through different stages: immature,
mature and hypermature. In the later stage cataracts may leak proteins
into the eye. These proteins can incite inflammation. The term for
inflammation inside the eye is uveitis. Lens-induced uveitis is
inflammation inside
the eye caused by a leaky lens. The eye has an allergic-like reaction
to
this lens material. Lens-induced uveitis can damage the eye leading to
complications such as glaucoma, retinal degeneration or retinal
detachment,
all of which can result in blindness.
Cataract Surgery
In cataract surgery the lens (cataract) is removed along with the front
part of the lens capsule. The capsule covering the back of the lens is
usually left in place to maintain the normal arrangement of the
structures in the eye. In some cases an intraocular lens implant may be
inserted to improve close-up vision after surgery.
To perform cataract surgery the patient must be under general
anesthesia. Then, an incision is made in the cornea and the lens is
removed. Two
types of surgery are used in animals. In most cases a small incision
is made and phacofragmentation performed. Phacofragmentation (also
called
phacoemulsification) utilizes hi-frequency sound waves to break up the
lens and then the small fragments are removed.
The second type of surgery is performed in cases where the lens is too
hard to be broken up by the phacofragmenter. Very old animals may
need this type of surgery. A larger corneal incision is made and after
removal of the capsule, the lens is gently expressed from the eye in
one
piece.
Patient Selection and Preparation
In order for your pet to be considered for cataract surgery, he or she
must be relatively free of serious illnesses, skin disease and dental
disease. Pre-operative blood tests are performed in all animals to help
rule out any undetected kidney or liver problems.
In order for your pet to benefit from surgery, the retina, the tissue
in the back of the eye that receives light, must be intact and
functioning. Ocular ultrasound is performed before surgery to make sure
the retina
is attached. An electronic retina test called an electroretinogram
(ERG),
is also performed to make sure the retina is functioning well enough to
go ahead with surgery.
Owner Participation
After cataract surgery, you will have a lot of work to do to help
achieve a successful outcome. Several types of eye drops need to be
given 4 times a day for at least a few weeks after surgery. Also, oral
medications are given for a few weeks after surgery. Eventually these
medications are decreased, discontinued or used in very small amounts.
Sometimes, however, an animal may need some medication for extended
periods of time.
An Elizabethan Collar is necessary for two weeks to keep your pet from
rubbing its eyes after surgery.
Several recheck visits are required after surgery. Typically there are
2-3 visits during the first two weeks following surgery and then
every few weeks- months for the first 6 months. Then we may recommend
rechecks 1-2 times per year. These rechecks are necessary to detect and
avoid any complications of surgery that may decrease vision.
see also Cataracts-fred
Lanting
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NUCLEAR SCLEROSIS
Nuclear Sclerosis is a normal aging change of the lens. The lens
is made up of several layers of cells arranged somewhat like the layers
of an onion. Layers of cells are added continually throughout the
animal's life. As your dog or cat gets older, new layers are added and
the cells become packed together more tightly in the center of the lens
(the nucleus). The increased density of the lens causes it to look more
cloudy in dogs over seven years of age. The lens will become
increasingly cloudy as the animal ages, but it almost never has an
effect on vision.
Nuclear Sclerosis should not be confused with CATARACT (a complete
opacity of the lens). A cataract is a different problem that is also
characterized by a cloudy lens. While a cataract is an abnormality that
can cause blindness and irritation inside the eye, nuclear sclerosis
is normal for an older dog, and the condition usually does NOT
interfere
with vision! There is no medical treatment that will cure wither a
cataract
or nuclear sclerosis. Surgical removal of a cataract may be indicated
to regain vision, but surgical removal of a lens with nuclear sclerosis
would not be helpful.
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Lens
Luxation
The lens of the eye is
the clear structure which focuses the image onto the retina. When the
lens
pathologically loses it's clarity, we call it a cataract.
The lens is located behind the iris, the central portion being exposed
by the pupillary opening. The lens is normally held in position by
small fibers called zonules, or the suspensory ligaments. The zonules
are attached to the equatorial perimeter of the lens and to the ciliary
body to keep it in position. Aqueous fluid (aqueous humor) fills the
anterior chamber of the eye, and the vitreous, a jelly like material
fills the vitreous chamber behind the lens. The aqueous fluid is
manufactured in the ciliary body and flows through the pupil into the
anterior chamber and exits the eye through the ciliary cleft or
drainage angle where the cornea and the root of the iris meet in the
periphery of the anterior chamber. Here, the aqueous fluid re-enters
the general circulation of the body. The aqueous humor maintains the
normal pressure of the eye known as intraocular pressure (IOP). A
disruption or blockage of the flow of the aqueous fluid often results
in glaucoma.
What is a Luxated Lens?
Should the zonules break the lens can either become loosened
(subluxated) or completely detached (luxated). When the lens completely
tears free of its zonular attachments and falls forward into the
anterior chamber, we call this an anterior luxation. It is also
possible for the lens to luxate posteriorly into the vitreous body.
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(a)
normal lens position
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(b)
anterior luxation forcing the iris forward. This results in a very
shallow anterior chamber
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(c)
lens is partially through the pupil. If the lens touches the cornea,
edema of the cornea will result
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(d)
complete anterior luxation. The anterior chamber is very deep as it
contain the whole lens. Pupillary block is present.
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Several causes of zonular
rupture are recognized.
Primary (heritable) lens luxation seen in many Terrier breeds.
Secondary to trauma
Secondary to inflammation (uveitis)
Secondary to glaucoma
Congenital due to abnormal development
Idiopathic
Breeds with heritable lens luxation
Australian Cattle Dog Bedlington Terrier Border Collie Brittany
Spaniel Deutsche Jadgterrier Fox Terrier German Shepherd Jack Russel
Terrier Manchester Terrier Miniature Bull Terrier Norwegian Elkhound
Scottish Terrier Shar-Pei Tibetan Terrier Welsh Terrier West Highland
White Terrier Whippet . .
Since lens luxation may cause glaucoma, and since glaucoma may cause
lens luxation it is important to determine which disease came first.
When lens luxation occurs secondarily to glaucoma, it usually occurs
late
in the disease once the elevated pressure within the eye has caused the
sclera to stretch, and the zonular ligaments to tear. This does not
occur
until long after vision has been lost. In such a case, attention must
be given to resolving the pain associated with glaucoma.
What happens when the lens luxates?
An anteriorly luxated lens is extremely serious, because it blocks
the flow of the aqueous fluid in the eye. This often results in the
acute onset of glaucoma. We often use the term pupillary block glaucoma
since the luxated lens itself and some displaced vitreous obstructs the
flow of aqueous through the pupil. There are, however, other causes of
pupillary block glaucoma. In dogs, it is generally accepted that within
72 hours, the elevated pressure in the eye will cause irreversible
damage to the optic nerve and retina. In addition, the anteriorly
luxated lens may cause corneal damage by injuring the endothelial layer
of cells which help keep the cornea clear. Corneal edema of varying
severity may be the result.
A posteriorly luxated lens can also cause glaucoma since the vitreous
is displaced forward and can block the drainage angle.
Treatment
The first step in planning treatment for a dog or cat with a lens
luxation is a careful assessment of the prospect for vision in the eye.
If the lens luxation is longstanding and if there is glaucoma greater
than 72 hours in duration, or if there is hemorrhage in the eye the
chances
of saving vision is reduced. If the lens luxation is recent, and if the
glaucoma is not severe, and the retina and optic disc still look
healthy,
then there may be a reasonable chance of saving vision with surgery. In
this case the surgery done is called an intracapsular lens extraction
where
the lens is removed with its capsule or covering intact. This requires
a
larger incision into the eye than traditional cataract surgery, and
since
the lens capsule is being removed, it is difficult, but not impossible,
to replace the lens with an artificial lens (IOL). In many cases, it is
also necessary to remove some of the vitreous which has also herniated
forward.
This is called a vitrectomy.
In some cases the patient is presented with the lens subluxated
(partially luxated). If there is no pupillary block or glaucoma
present,
then medications may be used in an effort to keep the pressure low, and
to keep the pupil relatively constricted to reduce the chance of
anterior
luxation. In some cases, where mild or intermittent glaucoma is
present,
laser surgery may help stabilize the intraocular pressure. Frequent
re-examinations
are required as the situation may change to true luxation in some cases.
If the eye has been blinded as a result of the glaucoma caused by the
lens luxation, then emergency lens removal surgery will not benefit the
situation. If the eye is painful, something must be done to relieve the
pain. The two main solutions (also discussed on the glaucoma page),
are enucleation (removal) of the eye, or an intrascleral prosthesis
procedure where the contents of the eye are removed and replaced with a
silicon ball, in many cases resulting in a comfortable blind eye with a
very reasonable cosmetic appearance.
What about the other eye?
Examination of the fellow eye, especially in the terrier breeds
predisposed to lens luxation may reveal a looseness or wobble to the
lens as the head moves. This is due to weakness in the zonular
ligaments
and in such a case future luxation is likely. In these cases,
preventative
lens removal may be best, in an effort to prevent a crisis. Medical
management
by an observant owner is also an option, but should lens luxation
occur,
emergency surgery will be required.
What about future generations?
Dogs affected with primary lens luxation should not be used for
breeding. Since this is a late onset disease, the breeder may encounter
a situation where a dog who has already produced a number of litters
of pups develops a lens luxation. This is disconcerting since it would
be advisable not to use any of the second generation for breeding
either.
Routine eye certification examinations will not, in most cases, detect
a dog predisposed to lens luxation, unless the ligaments have already
started to weaken and the slight wobble of the lens is detected by the
ophthalmologist during the examination.
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CORNEAL
DYSTROPHY
Julie
Gionfriddo DVM, Dip.ACVO, ACVO Genetics Committee/CERF Liaison.
Michael Zigler DVM, CertVOphthal.
Distinction between Corneal Dystrophy and Corneal Degeneration
Confusion often arises over the use of the term "corneal dystrophy" in
dogs. Technically, "corneal dystrophies" are diseases of the cornea
that are bilateral, non-inflammatory and inherited 1,2. The confusion
arises because the term "corneal dystrophy" is sometimes used to refer
to a disease with similar clinical signs but is not hereditary. A more
appropriate term for the non-inherited conditions is corneal
degeneration.
Clinical Appearance
In most breeds, corneal dystrophy appears as gray-white, crystalline or
metallic opacities in the center of the cornea or close to the
periphery. These opacities may affect any layer of the cornea, the
epithelium (outer layer), the stroma (the thick, middle layer), or the
endothelium (the
inner layer). The opacities are usually oval or round and are sometimes
doughnut-shaped. The age of onset of the disease varies within and
among
dog breeds and may range from 4 months in Airedale Terriers, to up to
13
years in Chihuahuas. The opacities usually progress but in some cases
they remain static. Their progression may be very slow and may or may
not lead to blindness (common in Cocker Spaniels, Poodles, Samoyeds,
Siberian
Huskies, Pointers, German Shepherds, and Bichon Frises). On the other
hand, progression may be rapid and lead to blindness (more common in
Airedale
Terriers, Boston Terriers, Chihuahuas and Dachshunds) 2. The mode of
inheritance
varies among breeds and in many breeds it is unknown. In the airedale
terrier it is thought to be a sex-linked trait 1,3 and in the Siberian
Husky, Corneal Dystrophy has been shown to be a recessively inherited
trait
with variable expression 4.
Corneal dystrophies are usually not painful. In a few breeds, however,
a dystrophy can lead to secondary breaks in the epithelial (outer)
layer of the cornea. When this occurs a painful corneal ulcer develops
requiring intense treatment. In other breeds, a painful ulcer may not
develop and the dystrophy itself is not treatable. No medication will
"dissolve" the opacity. Surgical removal of the dystrophic area may
temporarily decrease the opacity in cases of epithelial dystrophy.
Often, however the opacities will reform in the healed cornea.
Characteristics of corneal dystrophy in 6 dog breeds:
Shetland Sheepdogs have corneal dystrophy which may begin as
early as 4 months of age and usually progress throughout life 5. It
usually manifests as small gray or white rings which start in the
center of the cornea and later other spots develop peripherally. This
condition is an epithelial dystrophy, meaning it is in the superficial
layer of the cornea. This corneal dystrophy is inherited but the mode
of inheritance is unknown. In Shelties this disease can cause corneal
ulcers.
In Beagles, corneal dystrophy may begin as early as 3.5 years of
age 6. Beagles usually have either an anterior stromal opacity or one
which involves all layers of the stroma. The opacity progresses from an
oval "nebula" (cloud-like lesion), to a racetrack-shaped lesion, to an
arc-shaped opacity. In Beagles dystrophy rarely causes corneal ulcers
and the mode of inheritance is unknown.
Siberian Huskies have a form of corneal dystrophy which is
properly called "crystalloid corneal dystrophy." it is inherited as a
recessive trait and appears round or horizontally oval 4. It begins as
a diffuse, gray haze in the anterior stroma and may progress to
crystals
or gray-brown smudgy deposits in the anterior stroma, or involve the
posterior
part of the stroma or the entire stroma 2. This form of dystrophy
usually
begins between 5 and 27 months of age.
Boston Terriers and Chiuhuahuas have a form of endothelial
dystrophy which usually begins later in life (5 to 9 years) 7. Its mode
of inheritance is unknown. This disease begins as a fluid build-up
(edema) in the cornea due to the inability of the endothelium to act as
a water barrier to keep the fluid inside the eye from percolating into
the corneal stroma. The fluid build-up causes the cornea to look white.
It begins
at the edge of the cornea, progresses centrally and often involves the
entire cornea, causing the cornea to appear thickened. The fluid can
accumulate under the epithelium and lift it off, thus causing a painful
corneal ulcer which is very difficult to treat.
Airedale Terriers have a dystrophy which is presumably
sex-linked inherited and affects male dogs as young as 9-11 months of
age. It is located in the anterior stroma of the cornea and consists of
an infiltration of lipid (fat). This form of dystrophy often progresses
to decreased vision by 4 years of age and is not treatable.
References
Cooley, P.L. and Dice, P.F.: Corneal dystrophy
in the dog and cat. Vet Clin No Am 20:681-692, 1990.
Whitely, D.: Canine cornea. In. Gelatt KN, editor. Veterinary
Ophthalmology 2nd ed. Pages 307-356; 1991.
Dice, P.F.: Corneal dystrophy in the Airedale. Proc Am Coll Vet
Ophthalmol. 7:36, 1976.
Waring, G. O.; MacMillan, A; Reveles, P.: Inheritance of crystalline
corneal dystrophy in Siberian Huskies. J Am Anim Hosp Assoc 22:655,
1986.
Dice, P.F.: Corneal dystrophy in the Shetland Sheepdog. Am Coll
Vet Ophthalmol, 15:241, 1984.
Ekins, M.B.; Waring, G.O.; Harris, R.R.; et.al.: Oval corneal opacities
in Beagles, PartII: Matural history over 4 years and study of tear
function. J Am Anim Hosp Assoc 16:601, 1980.
Dice, P.F.: Corneal endothelial-epithelial dystrophy in the dog. Am
Coll Vet Ophthalmol 7:36, 1976.
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RETINAL DYSPLASIA AND RETINAL FOLDS
Written
by Dr. Julie Gionfriddo, D.V.M., Dip. A.C.V.O.
Anatomy and Physiology
The retina is the neurological structure in the back of the eye which
receives light and converts it into an electrical signal. This
electrical signal is transmitted to the brain by way of the optic nerve
and is interpreted by the brain as vision. The embryological
development of the retina is quite complex. It forms from a small part
of the front of the primitive neural tube, the structure that becomes
the nervous system (brain and spinal cord) of the adult. Malformations
of the retina before birth are rare but can
be due to either hereditary or environmental (in the uterus) influences.
Pathology
Retinal dysplasia is a type of retinal malformation. The word
"dysplasia" simply means "a defective development of an organ or
structure". Retinal dysplasia occurs when the 2 primitive layers of the
retina do not form together properly. Mild dysplasia manifests as folds
in the inner retinal layer.
These are called "retinal folds". In "geographic" retinal dysplasia
there
are larger areas of defective retinal development. In the severe form
of
dysplasia, the 2 retinal layers do not come together at all and retinal
detachment
occurs. Retinal dysplasia is not progressive. It is a congenital defect
and animals are born with as severe a condition as they will ever get.
Retinal dysplasia can be detected as early as 6-8 weeks on a CERF
examination.
However, because the size of the eye is small and young puppies are
often
wiggling during examination, a 6 month recheck is recommended in order
for
the ophthalmologist to better see the back of the eye. The cause of
retinal
dysplasia in most breeds is genetic although prenatal infections with
herpesvirus
and parvovirus may also lead to it.
Affected Breeds
Retinal dysplasia is reported in 25 of the 100 breeds of dogs listed in
the 1996 edition of the CERF book Ocular Disorders Presumed to be
Hereditary in Purebred Dogs. Twenty-four of these breeds had retinal
folds reported, and 11 had geographic areas of dysplasia and/or retinal
detachment. Simple autosomal recessive inheritance has been suspected
in Akitas, American Cocker Spaniels, Australian Shepherds, Bedlington
Terriers, Beagles, Dobermans, English Springer Spaniels, Labradors,
Rottweilers, Old English Sheepdogs, Sealyham Terriers, and Yorkshire
Terriers. The means of inheritance has not been determined in many
breeds. In Labradors and Samoyeds a combination of retinal dysplasia
and skeletal defects has been described. This condition is known as
oculoskeletal dysplasia. In this condition an autosomal dominant gene
is thought to be responsible for the genetic defects. Homozygous
animals have skeletal changes and mild to severe retinal dysplasia
while heterozygous animals usually have mild retinal dysplasia.
Retinal folds rarely cause vision problems for the individual dog. They
represent small blind spots which are probably not even noticed by the
dog. However, large areas of dysplasia (geographic dysplasia) may lead
to large deficits in the visual field and dogs with retinal detachments
are completely blind.
There have been many questions recently about the certifiability of
dogs with retinal folds. Retinal folds may be seen in many breeds and
still pass a CERF examination and receive a CERF number. This is due to
the fact that the condition is thought either not to be hereditary in
the particular breed or has never been shown to be connected to serious
(blinding) forms of dysplasia. In some breeds, particularly Labrador
Retrievers, Samoyeds, and English Springer Spaniels, individuals with
retinal folds are NOT given a CERF number. Since retinal dysplasia is
common in these breeds and dogs and bitches with retinal folds can have
puppies with blindness and/or skeletal problems the gene should not be
perpetuated. In all breeds, individuals with geographic and retinal
detachment forms of retinal dysplasia are NOT certifiable.
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UVEITIS
Inflammation
of the Eye
written by Dr. Dennis Hacker
Edited by Dr. Michael Zigler
To understand what uveitis is and how serious it is, it is helpful
to know basic anatomy of the eye. The outer layer that encloses the eye
is composed of the clear cornea and the white sclera. The innermost
layer
is the nerve layer or the retina. The middle layer (uvea or uveal
tract)
is the nutritional layer rich in blood vessels. It is made up of: the
iris (colored portion in the front part of the eye), the ciliary body
that produces the fluid inside the eye (aqueous humor) and the choroid
that provides nutrition to the retina inside the eye. When inflammation
attacks specific segments of the uveal tract the disease is further
classified depending on the affected structure. Iritis is inflammation
of the iris. Cyclitis is inflammation of the ciliary body. Anterior
uveitis or iridocyclitis is inflammation of both the iris and ciliary
body. Choroiditis or posterior uveitis is inflammation of the choroid.
If all three structures (iris, ciliary body and choroid) are
inflamed then it is called panuveitis.
Due to its rich blood supply, the uvea or uveal tract is a natural
target for diseases originating in other parts of
the body. Because the cornea is normally clear, signs of these
diseases may be seen first in the eye often before signs develop
elsewhere in the body. Additionally, uveitis may have causes within the
eye such as cataract or changes in the lens.
Click on photo to enlarge image
Diagnosis of Uveitis
Uveitis may cause vague clinical signs that can include blinking,
squinting, watery discharge, and fear of light (photophobia) without
any obvious
changes to the eye itself. The normally clear cornea may appear dull or
very blue due to uveitis. In other cases, the cornea becomes cloudy due
to white blood cells accumulating on the inside of the cornea. The
conjunctiva
(white of the eye) becomes red and swollen. In some cases of uveitis,
the
iris (coloured portion of the eye) becomes red or changes colour.
Uveitis
is usually diagnosed by an examination of structures of the eye using
instruments
that magnify and illuminate. In more advanced cases, changes are
visible
without special instruments. Once uveitis is diagnosed, a general
evaluation
of the patient should be performed if uveitis is suspected to be a sign
of internal disease. Blood profiles or other tests may be necessary if
a certain disease is suspected or to find the cause of the uveitis. An
ophthalmic examination consists of a visual inspection of the external
and
internal portions of the eye and the measurement of ocular pressure.
Ocular pressure is maintained by fluid (aqueous humor) which is
continually produced by the ciliary body and drains from the eye. If
the ciliary body is inflamed fluid production should slow down and the
ocular pressure
should drop. The aqueous humor produced in the eye flows through the
pupil
then drains into an 'angle' between the iris and the cornea where it
leaves
the eye. Cellular debris produced in uveitis can block this drainage
angle.
Alternatively, the iris may adhere to the lens and block fluid flow and
result in increased ocular pressure - glaucoma. Once uveitis resolves,
glaucoma may persist if drainage structures were permanently damaged by
the inflammation. Recheck of the eyes following the resolution of
uveitis
is important for this reason.
Causes of Uveitis
Uveitis may be caused by many different diseases. Diseases in the dog
include ehrlichiosis, Rocky Mountain Spotted fever, Lyme's disease and
brucellosis. In the cat, uveitis can be a consequence of Feline
Leukemia Virus (FELV), Feline Infectious Peritonitis (FIP), Feline
Immunodeficiency Virus or Feline AIDS (FIV), toxoplasmosis or other
diseases. In any animal, penetrating
injuries such as cactus spines, porcupine quills, pellets or b.b.'s or
a
scratch may result in uveitis. Inflammation of the uveal tract can
occur
when the lens leaks some of its contents into the eye. The lens may
cause
uveitis when injured, when a cataract is rapidly forming, when cataract
is
dissolving or following certain types of surgery. Further possible
causes
are local bacterial infection, immune mediated (autoimmune) diseases,
cancer
and parasitic diseases. Treatment can be more specific if the actual
cause
of uveitis is known. Unfortunately, in up to 75% of the cases the cause
of
uveitis is never determined.
Medical Treatment
Medical treatment of uveitis must be aggressive to prevent glaucoma, to
prevent scarring of the structures inside the eye and to prevent
possible blindness. Different medications are used to control the
original cause of the uveitis, if known, and to minimize the
inflammation itself.
Aspirin (not aspirin substitutes), indomethacin, Profenal(R) and
corticosteroids (cortisone drugs) minimize the inflammatory process.
Corticosteroids may be administered by injection under the conjunctiva
(movable white tissue of the eye), by eye drops, or as an oral
medication depending on the location of uveitis. Eye drops are most
often used for anterior uveitis. Injections and oral medication are
used for posterior uveitis or panuveitis. Drops in the eye must be
postponed if damage to the corneal surface is present (ulcer) because
the corticosteroids prevent healing of the ulcer or lead to a worsening
of the ulcer. If certain systemic diseases are suspected, oral
corticosteroids may be postponed until laboratory test results become
available. Aspirin can be used in dogs and cats by mouth and helps
reduce inflammation. Indomethacin or Profenal(R) drops are a
non-steroidal anti-inflammatory agent that will help reduce the
inflammation of the eye.
Dilating drops or ointments widen the pupil and relax the muscles
within the eye. These two actions result in fewer adhesions and less
pain for
the patient. This medication may not be used if glaucoma is present as
it may further decrease the fluid drainage from inside the eye and lead
to increased pressure.
Oral and topical antibiotics are only given when a bacterial infection
is present within the eye. Antibiotics are not often used as bacterial
infections are not commonly found as the cause of inflammation.
Prognosis
The treatment of uveitis requires therapy to halt the inflammation
of the uveal tract along with a search for the cause of the condition.
Diagnostic tests may be needed to determine possible causes. The
results
of these tests are very important for proper treatment to be given.
Follow-up
examinations ensure optimal therapy is being given and guard against
possible
complications. Uveitis, if caught early and treated diligently and
aggressively,
will often resolve without serious consequences. Unfortunately, in
certain
individual patients the cause of uveitis is never determined and
treatment
may be life-long. In other patients, the uveitis is so severe that
removal
of the eye is necessary.
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This information is provided by Provet for educational
purposes only.
You should seek the advice of your veterinarian if your pet is ill
as only he or she can correctly advise on the diagnosis and recommend
the treatment that is most appropriate for your pet.
Melanoma of the eye occurs in both cats and dogs, but there are
some significant differences between these tumours in the two species.
The main differences between melanoma of the eye in cats and dogs are
as follows :
|
CAT
|
DOG
|
Frequency of occurrence
|
Uncommon
|
Uncommon - but it is the most
common intraocular neoplasm in dogs
|
Most common site
|
Iris (anterior face usually)
|
Iris (anterior surface) or ciliary
body (difficult to see in early stages).
|
Most common form
|
Diffuse infiltrate
|
Diffuse infiltrate Raised nodule
|
Colour
|
Brown usually
|
Brown to black
|
Rate of growth
|
Often very slow.
|
It can take months-years before
secondary effects develop. Slow
|
Secondary effects
|
Glaucoma.
|
Corneal oedema, glaucoma, lens
luxation
|
Predisposed breeds
|
|
German Shepherd Dogs, Labrador
Retrievers
|
Genetic inheritance
|
|
Possibly
|
Metastatic spread
|
High - 30-60% spread
|
Usually less than 5% spread
post-enucleation follow-up.
|
Treatment Enucleation.
|
Laser treatment? Enucleation.
|
Surgical resection occasionally.
Laser treatment ?
|
Differential diagnosis
|
Melanosis of the iris in
middle-aged cats can be difficult to differentiate
|
|
Metastasis
|
Radiograph chest for secondary
spread
|
Radiograph chest for secondary
spread
|
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The above information is simply
informational. It's intent is not to replace the advice of a
veterinarian nor to assist you in making a diagnosis of your pet.
Please consult with your own veterinarian for confirmation of any
diagnosis. Your pets life may depend on it.
