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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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Iris
Coloboma
VP Client Information
Sheets
By VIN Community Contributors
The iris is the
part of the eye that’s colored. In dogs, the iris is usually brown or blue.
In cats, it can be brown, blue, green, and gold (yellow). The pupil, which
is the black hole in the center of the iris, controls how much light gets
into the eye to the retina.
Coloboma means a thinning or a hole in the eye structure. In this context,
it is an indication of how thin the iris is. The animal is born with the
coloboma; it’s an area of the iris that never formed properly. Large holes
allow more light to enter the eye through the pupil, resulting in squinting.
The coloboma can be mild or severe. In severe cases, there is a sort of notch
in the margins of the pupil.
The iris coloboma, which is relatively common, does not affect vision,
and it does not progress to anything else. Unless your affected pet herds
sheep or cattle, this sensitivity to light is not a big problem. Nothing
can be done to treat it, although it’s possible to buy dog goggles (Doggles®)
that function as sunglasses, and reduce the squinting. (Most cats would rather
not wear such goggles.)
Most congenital (born with) iris colobomas are genetic. Affected dogs
or cats should not be bred. It is one of the
things dogs are screened for during a Canine Eye Registration Foundation
(CERF) exam. When eye exams are given, the irises will be examined both before
and after the eyes are dilated, as some small colobomas might not be seen
after dilation. At the present time, cat registries do not screen for this.
If you are getting a purebred puppy from a breed known to have iris colobomas,
ask the breeder for a CERF rating from each of the parents. It is seen most
commonly in Australian Shepherds, but other breeds can have it also. Iris
colobomas are associated with merle to merle breeding. (Merle to merle breeding
produces numerous vision and hearing problems.)
Although the coloboma itself is not a real problem, other problems associated
with it (cataracts, lens colobomas, retinal colobomas, etc.) can cause vision
problems. Some of those problems can be treated. The coloboma alone will
not cause health problems, but it’s best to keep an affected animal with a
severe case out of bright sunlight.
Copyright
2007 - 2007 by the Veterinary Information Network, Inc. All rights reserved.
This work was originally published by Veterinary
Information Network, Inc.(VIN)
and is republished with VIN's permission.
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THE PET HEALTH LIBRARY
A syndrome is a collection of
symptoms that have meaning when they go together. It is important to realize
that having a syndrome is not the same as having a diagnosis. A syndrome,
however, often has a limited number of causes such that recognizing a specific
syndrome brings one substantially closer to a specific diagnosis.
What is Horner's Syndrome?
Horner's syndrome consists of five signs:
Constricted pupil
Elevation of the third eyelid
Retraction of the eyeball into the head
Slight drooping of the eyelid
Increased pink color and warmth of the ear and nose on the affected side
(very hard to detect in small animals)
All these signs are caused by damage to sympathetic nervous system as
it supplies the eye on the affected side of the head.
What is the Sympathetic Nervous System?
Our bodies have numerous functions that are controlled by our nervous
systems yet we are completely unaware of them. Our heart and respiratory
rates, the amount of sweat and other secretions we produce, circulation
to different body areas, pupil dilation and constriction are all regulated
by our nervous systems automatically and without our knowledge or control.
The part of our nervous system dedicated to these automatic systems is called
the autonomic nervous system.
The autonomic nervous system is divided into the sympathetic nervous system
and the parasympathetic nervous system. The parasympathetic system maintains
a status quo, normal, business as usual state; the sympathetic system prepares
the body for a fight or flight situation. Some changes that might be stimulated
by the sympathetic system include: increased sweating, dilated pupils, increased
heart rate, and increased blood flow to muscles. Both systems coexist in
balance in the healthy body.
When the sympathetic system controlling one of the eyes is damaged, only
the parasympathetic nerves work and Horner's syndrome is created.
How Can the Sympathetic Damage Occur?
The nerve carrying the tiny nerve fibers that provide sympathetic control
to the eye have a long path and the damage may have occurred anywhere along
this path.
The nerves originate in the spinal cord in the patient's neck. They exit
the spinal cord just inside the chest and travel up the neck to the head.
These nerves then connect to new nerves just below the ear. The new nerves
continue their journey to the eye. The damage can occur in the neck area,
the ear area or the eye area. Damage can occur in the form of trauma, tumor
involvement, infarction (abnormal blood clot), middle ear infection, or diseases
of the eye itself.
Sorting it Out
Localizing which area of the sympathetic nerve system is affected goes
a long way in determining the nature of the damage as different areas of
the system are prone to different types of injury. Special eye drops can
be used to stimulate different areas of the nervous system and determine
if the lesion is in the first nerve segment or in the second nerve segment.
Most are in the second nerve segment.
With second nerve segment involvement: If ear infection is not obvious
and disease of the eye beyond the Horner's syndrome itself is not obvious,
then it is probably prudent to allow the syndrome to resolve on its own.
This usually occurs within 6 to 8 weeks. Further diagnostics may be undertaken
if new developments occur or if the syndrome persists beyond this time.
With first nerve segment involvement: Involvement of the first nerve segment
indicates a problem in the chest or spinal cord and is more significant.
Chest radiographs should be taken to rule out cancer spread to the chest (the
only sign of this may be the Horner's syndrome). The front leg should be
carefully checked for evidence of function loss as a tumor or protruding intervertebral
disc could be exerting pressure on the spinal cord. Trauma to the neck as
with a strong jerk from a collar or straining against a leash can also produce
Horner's syndrome from this section of the nerve. Generally more diagnostic
work is needed for cases involving the first nerve segment as there is potential
for more serious underlying causes. If the syndrome stemmed from pulling
on the leash, it should resolve uneventfully depending on how badly damaged
the nerve is.
Treatment
It is not necessary to treat Horner's syndrome. The syndrome is not painful
and does not interfere with vision. The significance of the syndrome is that
it indicates nerve damage which must be recognized. If one wishes to treat
the syndrome for cosmetic reasons, phenylephrine eye drops can be prescribed
to relieve clinical signs.
Causes of Protrusion of the Third Eyelid
I am commonly asked about animals with protruding third eyelids. Possible
reasons for the third eyelid to become prominent include the following.
Horner's Syndrome
Usually only one eye is involved although it is possible for both eyes
to be involved. As described above, there are additional features of this
syndrome.
Tetanus
With this disease, the third eyelids tend to "flash" up as if to replace
normal blinking. Twitching and stiffness are also features and are worse
if the animal is startled. Event hough this is the result of an anaerobic
infection of a wound by Clostridium tetani, most owners are not aware of the
wound (which may have appeared to heal even weeks before). Cats are resistant
to tetanus so this would be an unusual cause of third eyelid elevation in
a cat.
Facial Paralysis
The facial nerve controls the movements of facial expression including
blinking. To protect the eye, the third eyelid may come up and the eye may
be pulled back in the socket somewhat. Facial paralysis commonly results
from severe ear infections.
Haws Syndrome
Animals, particularly cats, may bring up their third eyelids in response
to illness, particularly intestinal irritation. Generally the third eyelid
remains elevated for 4 to 6 weeks and eventually goes back to normal.
Facial Muscle Atrophy
With loss of muscle in the face, particularly the chewing muscles, there
is nothing to hold the eye in its normal position and it will sink slightly
into the socket and the third eyelids will ride up.
Dehydration
In this situation dehydration must be fairly severe. The eyes sink into
their sockets and the third eyelids ride up.
Shrinkage of the Eye
A diseased eye will shrivel up and become very small. The third eyelid
will have nothing to hold it down and will ride up.
Feline Dysautonomia (Key-Gaskell Syndrome)
This is a rare neurologic disease which features dilated pupils, elevated
third eyelids, constipation, urine retention, and other issues. This is a
severe disruption of the sympathetic nervous system and prognosis is very
poor.
If your pet's third eyelids protrude, please see your veterinarian
to sort out these possible causes.
Copyright
2004 - 2007 by the Veterinary Information Network, Inc. All rights reserved.
This work was originally published by Veterinary Information Network,
Inc. (VIN)
and is republished with VIN's permission.
**************************
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.
