What is involved in an ophthalmic examination?

by Dr. Dennis Hacker

When your pet is presented for an ophthalmic examination, several aspects of the examination are performed for every patient. Additional tests are employed when indicated. The examination will begin with the ophthalmologist taking a detailed history of the pet, its eye and what the client noticed and what previous medications have been used, if known. All this information will be entered into the patient's record either on a computer or on a paper record. Next, pupillary light reflexes are examined using a pen-light or a transilluminator. Doing this test tells if the retina is working and if all nerves are functioning normally.

The shining of the transilluminator into the eye of a cat to see the responses of the pupil. What is done next depends on what is seen during the initial cursory examination of the eye. If there is an ocular discharge, a test for tear production, known as a Schirmer Tear Test, will be performed.

Schirmer tear test strips are used to determine amounts of tearing from the eyes.

The strips are applied to the eye and allowed to sit for one minute and the amount of wetting is measured on the scale on the strip or on the packet.

Next, the anterior portion of the eye, as well as the eyelids, third eyelid and conjunctiva are examined using a slit-lamp.

In this shot, a handheld slit-lampis used to examine a feline patient.

If a defect in the cornea is suspected, fluorescein stain can be applied to the eye and the eye will be examined using a blue light to detect retained stain.

In this photo, the white arrow indicates the up-take of the fluorescein stain. The resulting area "glows" green when stimulated with a blue light. Occasionally, another stain, Rose Bengal, will be used to indicate damaged epithelial cells and not a loss of cells.

Next, the pressure within the eye will be determined to check for glaucoma. Here, a Tonopen-XL is used to acquire the intraocular pressure.

If necessary or indicated from previous tests, gonioscopy will be performed by applying a thick lens to the cornea and examining the area where fluid drains from the eye.

This is a normal iridocorneal cleft (as indicated by the white arrow) and the patient has normal eyes. Next, dilating medication is applied to the eyes and the patient will wait for about 20-30 minutes whilst the eyes dilate for fundus examination. Once the eyes have dilated, examination of the retina, lens and vitreous can be performed using a hand lens.

Using a hand lens and the indirect ophthalmoscope, the fundus is examined. Finally, the results of the examination are recorded in the patient's record, the client is informed of all findings and any problem areas are discussed.

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Cataract

by Dr. Dennis Hacker

What is a cataract?

The lens is a unique living ocular tissue that is usually clear or transparent and is referred to as 'the crystalline lens' in medical texts. The normal lens focuses light on the light-sensitive nervous tissue (retina) located in the back of the eye. The word cataract literally means "to break down." Doctors refer to any opacity (or cloudy change) of the lens that causes light to scatter as a cataract. Cataractous changes of the lens may appear as small insignificant pigmented, gray or white "dots"., microscopic "blisters", a "cracked glass" appearance, a diffuse haze, a "pearly" sheen, white streaks or a completely white lens. The cataract usually begins as small dots or microscopic blisters and progresses to involve larger areas of the lens. The rate of progression is difficult to predict and may be very slow or quite rapid. A cataract is different than the normal aging change that occurs in the lens which is called nuclear sclerosis. Nuclear sclerosis is in the very center of the lens and occurs in patients over 7 years of age. These are not cataracts! At times the cataract appears to worsen overnight. Cataracts may develop in one or in both eyes. If a large portion of the lens becomes white, it prevents images from reaching the retina and blurred vision results. When a light is shined into the eye of a patient with a complete cataract, the patient only sees a white light and no images can be seen.

This is a picture of a cat with cataractous lens. The cataract has liquified and the nucleus or center of the lens has sunk within the lens capsule. The arrow shows the nucleus.

What should I do if I suspect cataracts in my pet?

The first thing to do if your veterinarian indicates your pet may have a cataract of any size is to have your pet examined by a veterinary ophthalmologist. The lens is an important link of the total visual system, yet the health of the entire eye should be evaluated before the lens develops a complete cataract. Early evaluation of the eye with a cataract sometimes permits examination of the retina. If the cataract is complete or "mature," the retina cannot be directly examined and an ultrasound examination may be needed. At the time of the initial examination, the cataract may sometimes be identified as to cause, area of involvement and stage of progression. Not all cataracts lead to blindness. "Incomplete" cataracts may not impair vision significantly. If your pet has a cataract and has shown some visual loss, evaluation will include the consideration of and benefit of cataract surgery.

How do I know if my pet has a vision problem?

Our pets are creatures of habit and love to please their owners. If vision loss develops slowly over a long period of time, your pet may adjust to your home and yard. Pets in familiar surroundings may readily move about even when almost blind because they have learned where all objects are. Signs such as bumping into objects, failing to retrieve favorite toys and fear of being left alone may be signs of vision loss. These are especially significant if they occur within the pet¹s home or yard.

What causes cataracts?

The cause of cataracts is an area continually being studied. Cataracts may result from injuries to the eye, inflammation within the eye (uveitis), internal diseases that have an effect on the eye such as diabetes mellitus, metabolic conditions or certain foods, chemicals and drugs. Although it may be difficult to name the specific cause of a cataract, cataracts that develop in eyes free of signs of ocular disease are assumed to be inherited. Inheritance is the major cause of cataracts in dogs and cats.

Are there types of cataracts?

The type of cataract may not be important for deciding whether surgery may be performed. Cataracts may be classified by age of onset, physical appearance of the cataract or state of development of the cataract. What is the treatment for cataracts? There is no medical treatment known to slow the progression of, prevent the formation of or reverse the changes of cataracts. Surgery to remove the cataractous lens is the only known treatment in animals and man. Successful surgery can provide a return of vision.

Should my pet have cataract surgery?

Cataract surgery is generally restricted to those patients who are developing a cataract in both eyes. If one eye has a blinding cataract and the other eye has a rapidly developing cataract or if rapidly developing cataracts are present in both eyes, surgery is recommended so the patient will not completely lose vision. It is also important to consider whether the patient is a good candidate for anesthesia. With continued improvements in veterinary medicine and anesthesia, age alone does not limit the possibility of surgery. With the use of modern anesthetic agents, successful surgery is performed on dogs and cats 17-18 years of age and older. The over-all health of the patient needs to be assessed before surgery. This may include chest x-rays, EKGs, ultrasound of the eye, blood analysis or other procedures. Cataracts may be removed from one or both eyes during the same surgery. Finally, you are the one who hears all the information and decides if surgery will be performed to restore vision for your pet.

Is my pet a good candidate for cataract surgery?

Cataract surgery involves a period of intense treatment and care both before and after surgery followed by an extended period of low level therapy. If you are unable to provide this treatment, surgery is not recommended. Alternatively, if your pet will not or cannot be treated as required, he/she is not a good surgical candidate. Animals who "bite the hand that feeds it" don't do well after cataract surgery.

What will my pet see after surgery?

Patients benefit from cataract surgery because it will allow them to be able to move about without the fear of bumping into objects. As in people, the loss of the lens causes a loss of "up-close" visual acuity or sharpness. Without a lens, a pet may not have completely normal vision after surgery, but they do regain useful vision. The up-close image they see will be slightly larger and only partially focused so that the images will be much less distinct. Distant vision (over 6-to-8 feet) is usually normal. Our pets don't drive or play golf or tennis. Yet they need clear vision. Their need for sharp vision is not as necessary as it is for humans. Some veterinary patients appear visually handicapped without a lens yet most show no apparent vision difficulties. Due to the vision difficulties without lenses, we recommend replacement lenses be placed during surgery for the routine cataract surgery. These lenses are made to the same exacting specifications that are used in human medicine. The replacement lenses allow improved vision over a patient with no lenses.

What does cataract surgery involve?

The preparation for cataract surgery begins several days prior to the actual event. You will be required to apply drops to one or both eyes three times daily for three days. These drops are an antibiotic drop and a corticosteroid drop to reduce bacterial contamination and inflammation. An antibiotic will be given by mouth twice daily for three days before surgery. Cataract surgery is performed on an outpatient basis. The morning of surgery, the pressure of the eyes of your pet will be assessed and the area of fluid drainage will be examined to decide the type of postoperative medication that will be needed. If not previously performed, an ultrasound may be performed to examine structures inside the eye(s) that cannot be visually seen. Next, blood tests (if needed) will be performed, a physical examination given and a catheter is placed into a vein to facilitate the administration of drugs. Drops are placed in the eyes at specific intervals before surgery. General anesthetic is induced using the most modern agents. An electroretinogram [ERG] is then performed to determine that the retina is working normally and a reasonable chance for vision exists following surgery. This procedure is used if the cataract has progressed to the point that the ophthalmologist cannot assess the retina during the initial examination. If the ERG indicates that vision is not possible, then surgery is not performed and the patient is awakened. If the ERG shows that vision is possible, the patient is prepared for surgery and moved to the surgical center. During the surgical procedure, the pet's respiration, oxygenation level of the blood, heart rate and blood pressure will be monitored by the anesthetic technician. An EKG will be attached to your pet so that the heart can be assessed during surgery. Surgery is performed using an operating microscope and sophisticated microsurgical instruments. The actual surgical procedure may last 30-40 minutes and general anesthesia is normally for 60-120 minutes per eye. During recovery, your pet will be closely monitored and will be discharged from the hospital 2-6 hours after surgery. An Elizabethan collar (E-collar) is placed on the pet so they will not injure their own eyes during the first 7-to-14 days following surgery. Postoperative medications are used to reduce inflammation and to prevent infection. Eye drops are applied every 6 hours for the first 24 hours. Antibiotics and possibly other medications will be given by mouth twice daily. The first postoperative examination is scheduled for the afternoon the day following surgery. During that examination, the pressure within the eye will be examined, the eye is evaluated for inflammation, tear test will be performed and determination of possibility of infection will be made. Further examinations will be scheduled as needed to follow the progress of healing. Medication must be given at regular intervals. After the first two weeks, the chances of infection are very low and the antibiotics are discontinued. Inflammation is the main problem which must be overcome and controlled. Topically applied antiinflammatory agents, both steroidal and non-steroidal are given as frequently and as long as needed to control inflammation. It is possible, due to the fact that dogs and cats are great scar tissue formers, that treatment will be necessary for 6-to-12 months or longer. These treatments are usually once or twice daily and may be as infrequent as every other day. Some patients are completely off medication in 6 months. Each patient is an individual.

This patient was examined 24 hours following a successful surgery. The white arrow shows the artificial lens and the dark arrow shows the retinal blood vessels visible around the artificial lens.

Are there possible complications to cataract surgery?

The success rate in cataract surgery has improved markedly in the recent years with the advent of newer medications and microsurgical techniques. The success rate is 90-95%. This does not mean that if the surgery is not successful your pet will have 5-10% vision. It means that 90-to-95 pets out of 100 will have vision OR 5-to-10 pets will remain blind in spite of the surgery. Although the success rate has risen dramatically, there are still several complications that need to be anticipated in order to prevent them. Intraocular bleeding, elevation of intraocular pressures [glaucoma], extreme postoperative inflammatory response, adhesions and self-trauma are possible complications. The risk of anesthesia is extremely minimal. The chief problem which is treated on an on-going basis is inflammation (uveitis).

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Eye Certification Examination or C.E.R.F.

by Dr. Dennis Hacker

What does a CERF exam entail? What is tested for? How is it done? Which dogs should have it done?

An eye certification examination is done by a veterinarian specialized in ophthalmology. The pupils of the patient are dilated with eyedrops called tropicamide, or a tropicamide & phenylephrine combination, and once the pupil is well dilated the examiner will usually illuminate the eye with a penlight or transilluminator looking for major abnormalities. Then the eye is examined in detail with a slit-lamp biomicroscope. This detects any abnormalites located in the cornea, anterior chamber, lens and front most portion of the vitreous. The types of abnormalities that may be noticed during this part of the exam include distichia (extra eyelashes), imperforate puncta (not opened tear ducts), corneal dystrophy (cholesterol development in the cornea), persistent pupillary membranes (embryological remnants), cataract (opacity of the lens), persistent hyaloid remnants (another embryological remnant) and vitreal degeneration. Finally the retina or fundus is examined using an ophthalmoscope and a focusing lens that is held in the examiners hand that provides the examiner a clear view of all parts of the retina. The indirect ophthalmoscope is a device which sits on the examiners head providing optics and a light source. This part of the examination may reveal such problems as Progressive Retinal Atrophy (PRA), Retinal Dyplasia, colobomas, choroidal hypoplasia, optic nerve hypoplasia, retinal detachment, and certain vascular abnormalities. A CERF examination is a typical eye screening examination as described above but is only done by veterinary ophthalmologists who are board certified by the American College of Veterinary Ophthalmologists who then records his or her observations on a CERF (Canine Eye Registry Foundation) form. In other countries, veterinary ophthalmologists who are board certified in their own country will examine the eyes for breeding soundness, and will issue a certificate following the examination but this will not be a CERF form. The dogs which should have eye certification examinations include all dogs used for breeding if any recognized heritable eye disorder is known to be present in the breed. Puppies should be examined before being sold if the breed is known to have any heritable eye disorder which is early onset and may be recognised at an early age.

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Cherry Eye or Prolapsed Gland of the Third Eyelid

by Dr. Dennis Hacker

Within the folds of the lower eyelid a thin portion of tissue is present that is often called the "nictitans" or "third eyelid". The third eyelid is found in most domestic animals. A gland called the "gland of the third eyelid" or the "glands nictitans" or the "haw" is located on the surface of the third eyelid which faces the cornea (clear portion on the outer surface of the globe). The gland is a tear producing gland. This gland produces between 30 and 60% of the tears in the dog and cat. The gland is normally out of sight and held in position behind the third eyelid by a small ligament. A prolapsed gland of the third eyelid (or "cherry eye") is thought to be associated with a laxity of the ligament.

Cherry eye in a dog which is inflamed.

Cherry eye in another dog.

The main orbital lacrimal gland, located beneath a portion of the skull bone, produces the rest of the tears. Unfortunately, the amount of tears produced by each of these glands is variable. The longer the gland is in an abnormal position the greater risk that the gland will be damaged and not fully functional when it is tacked back into place. In years past, when a cherry eye occurred, it would be surgically removed. It is now known that should the main orbital lacrimal gland be damaged later in life no "backup" for tear production would exist if the prolapsed gland of the third eyelid is removed. Dogs that have had the gland of the third eyelid surgically removed have a greater risk of developing keratoconjunctivitis sicca (dry eye or KCS ) than dogs with intact third eyelid glands. Additionally, studies have shown that leaving the gland of the third eyelid in a prolapsed position results in a higher incidence of KCS than those patient in whom the gland is surgically replaced. Certain breeds of dogs develop KCS and cherry eye. These breeds (American Cocker Spaniel, English Bulldog, Shar Pei, Shih Tzu, Lhasa Apso, and Chow Chow) frequently develop KCS after removal of the cherry eye. In Burmese cats (which are susceptible to cherry eye) it appears that the gland of the third eyelid may be the only gland which produces tears. Surgical removal of the prolapsed gland in Burmese cats can result in a devastating total loss of tears. Dry eye is a serious eye condition that is difficult to treat, and requires life-long treatment. The chance of developing KCS is lessened by tacking the gland back into its normal position thereby keeping the gland functional. This is the most desirable way of handling "cherry eye". Tacking surgery performed by an experienced veterinary ophthalmologist has a failure rate of less than 5 %. Failure means that the gland will reprolapse and need a second surgery in about 5 cases out of 100. At Animal Eye Specialists we have had great success with the tacking procedure we use. The tacking surgery is certainly more expensive than surgically removing the gland. However, the cost of treating dry eye (examination and medication fees) is much higher over the life of the pet. Despite surgery, dry eye may develop later in life if damage occurs to all of the lacrimal glands. This damage is usually associated with an immune system dysfunction and its occurrence cannot be predicted. For further information about dry eye (KCS) please see the handout for that condition.

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Collie Eye Diseases

by Dr. Dennis Hacker

Collies like other breeds of dogs have a number of inherited eye defects. Some of these are quite severe while others are relatively minor. The important ones we think should be considered are Collie eye anomaly (CEA) and progressive retinal atrophy (PRA). COLLIE EYE ANOMALY Collie eye anomaly was first reported in 1953. The original report included a description of pale area in the retina due to a deficiency of blood vessels along with a bulging of the back of the eye and retinal detachments. Since the first reports a number of studies have been completed and tens of thousands of Collie dogs have been examined. Based on these studies and examinations, specific breeding recommendations have been proposed. CEA is the incomplete development of the eye that is present as early as the 28th day of development. The defect involves the sclera (white outer wall of the eye) and the choroid (blood vessel layer in back of the eye). Additionally, the retina (portion of the eye that turns light into electricity), the retinal blood vessels and the optic nerve are also involved. Clinically the severity of CEA is variable--ranging from no apparent vision defect to total blindness. It is found in rough and smooth Collies and all color coats are involved. Most Collies (80 to 90%) with CEA do not demonstrate vision problems. CEA is a simple recessive defect. This means that a gene from both mother and father (homozygous state) must be present for CEA to develop. Carrier animals (who have the gene from only mother or father) and normal animals cannot be separated based on an ophthalmic or eye examination. A number of researchers have attempted to separate the various aspects of the disease but were unable to do so. When the disease was first described, such a large percentage of the population was affected that a number of grading systems were devised to make classifications of individuals easier. It was the feeling of some people at the time that the severity of the disease might be lessened by breeding individuals with minor problems to each other. Certainly this idea has had its place in history of breeding better Collies. Unfortunately dogs with minor afflictions can and do produce severely afflicted offspring. Likewise blind parents can produce less afflicted offspring. An individual with a mildest problem is just as bad as a totally blind dog for the purpose of genetic selection. Because the grading system remains firmly entrenched within the Collie breeding community, a discussion of the grades and categories is appropriate

Grade	Findings
Grade1	torturous retinal vessels, extremely small areas of choroidal hypoplasia
Grade2	torturous retinal vessels, substantial areas of choroidal hypoplasi
Grade3	tortuous retinal vessels, substantial areas of choroidal hypoplasia (blood vessel loss) with pits (colobomas) or areas of out pouching (ectasia) in the posterior segment
Grade4	all the above defects with a retinal detachment
Grade5	all the above defects with a retinal hemorrhage

It is possible for one eye to have a different grade than the other but both eyes in almost all cases are affected. "Go normal" is a term used to describe an affected individual, Grade 1 or Grade 2, in which the area of choroidal hypoplasia fills in so it appears normal during later examinations. These animals act genetically like the affected individuals that they are. They can set a breeding program back years. Because the lesion is present at birth, puppy eyes can be checked as early as 5 to 6 weeks of age. For the ease of the examiner and to facilitate a more accurate exam, evaluation at 6 to 8 weeks is recommended.

PROGRESSIVE RETINAL ATROPHY IN THE COLLIE

Progressive retinal atrophy (PRA) is a collective term used to describe a variety of inherited retinal diseases in dogs. Within this category is a syndrome known as rod-cone dysplasia or PRA in the Collie. A dysplasia indicates an abnormal developmental process where tissue, in these cases the rod and the cones, never form normally. Clinically affected animals exhibit night blindness as early as 12 weeks of age and progress to total blindness by one year of age. All affected individuals become totally blind. Changes can be seen in appearance of the retina by 6 months. Late stages are characterized by a reduction of retinal blood vessels, increased reflection from inside the eye, pigment changes in the retina and a pale optic disc. An electroretinogram (ERG) is the recorded electrical changes in the eye over a time that results from a light being shined in the eye. ERG changes are evident as early as 1-to-12 weeks of age. The test involves placing a contact lens on the cornea to which a wire has been attached. Two other wires have been attached to the skin around the eye. These wires are then connected to amplifiers and an oscilloscope. A dim light is then flashed into the eye at various intervals using a variety of filters. It is possible to separate the rod and the cone function and differentiate affected puppies from normal animals before the onset of clinical signs. Rod-cone dysplasia (PRA) is inherited as a recessive gene. Therefore a homozygous individual (one who received a gene from both mother and father) is affected while the normal animals and carriers (who received a gene from either mother or father) appear normal and show no changes in vision or electroretinographic changes. A test is been devised to detect carriers short of test breeding. Unfortunately, the test will not be available for quite a few years. Test breeding involves breeding of suspected patients to known afflicted individuals. Because the disease is expressed in the homozygous form only the production of affected offspring indicates that the suspected individual is a carrier. Statistically the more normal individuals produced as a result of test breeding the greater the assurance the suspect is a normal dog or a non-carrier. At least 6 puppies must be produced from the suspected individual to have a 95% level of confidence that the suspect is normal and a non-carrier.

MERLE COLLIES

The fundus of the Merle Collie presents a special challenge in differentiating affected individuals from non-affected in terms of Collie eye anomaly. The Merle fundus is often lightly pigmented and exhibits a normal amount of choroidal hypoplasia (loss of blood vessels). Some of these individuals cannot be designated as normal based on a clinical examination. Test breeding or an ERG may be required.

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Feline Corneal Sequestrum

by Dr. Dennis Hacker

What is a sequestrum, anyway?

To understand corneal sequestrum , we first need knowledge of the anatomy of the cornea (clear portion of the eye). Covering the outside of the cornea is a layer of epithelium. This epithelium is much like our skin cells, but it usually isn't pigmented and doesn't have hair or blood vessels in it. In the cat, the epithelium is about 6-8 cell layers thick. Lining the inside of the cornea is one cell layer called endothelium. These endothelial cells are 'leaky' and allow fluid from the inside of the eye (aqueous humor) to leak into the corneal tissue and then pumps it back into the front of the eye. This pumping mechanism keeps the cornea clear. The greatest portion of the thickness of the cornea (about 90%) is the 'stroma' which is a collagen fiber matrix. The cornea in the cat is approximately 0.6 mm thick. (For comparison, a dime is approximately 1 mm thick.)

Corneal sequestrum is a condition peculiar to the cat in which the corneal stroma dies and then degenerates. This condition is called necrosis. The dead stroma becomes pigmented and becomes irritating to the body causing pain and blood vessels to enter the stroma. There is often corneal edema and white blood cell infiltration as a 'foreign body' reaction to the necrotic tissue occurs. Various names have been given to this lesion since it was first described in 1965. These include corneal mummification, the 'isolated black lesion', corneal nigrum, keratitis nigrum, focal degeneration of the cornea, corneal necrosis, primary necrotizing keratitis and corneal sequestration or sequestrum. The cause of the corneal sequestrum is unknown. A few veterinary ophthalmologists suggest primarily corneal abnormal development.

Other ophthalmologists suggest that the dead tissue is secondary to a host of factors which cause corneal irritation. Factors such as herpesvirus, lack of tear production (keratoconjunctivitis sicca or KCS), chronic corneal ulceration and foreign objects in the eye have all been suggested as causes of corneal sequestrum. Additionally, some of these cats sleep with their eyes open (lagophthalmos) , and the tear film is not spread adequately over the central cornea which results in drying. Some affected cats have a subtle inrolling of the lower eyelid (entropion) which may irritate the cornea. The origin of the black discoloration of the necrotic stroma is thought to be products in the tears which adsorbs into the degenerative tissue.

Which cats get this condition?

Corneal sequestra are seen in cats of all ages except the newborn Although sequestra (plural of sequestrum) most often occurs in young adult cats, we have seen it in cats from 2 to 16 years of age. There is no difference in occurrence by sex of the cat, but there is a noticeable breed distribution:

Incidence of Corneal Sequestrum by Breed:

• Himalayan 35%
• Persian 35%
• Siamese 15%
• Domestic 10%
• Abyssinian 5%

The Persian, Siamese and Himalayan are most often seen, but cases also occur with lesser frequency in the Exotic Shorthair and Domestic Shorthair breeds. This breed predisposition may not be genetic, as these breeds share certain conformational features that may predispose the cat to corneal sequestration. These breeds have some degree of lagophthalmos (their eyes protrude), and thus are subject to additional risk of trauma.

What will I see when a sequestrum occurs?

The usual clinical presentation is a cat with a history of chronic eye problems. Most affected cats exhibit blepharospasm (excessive blinking or squinting), tearing and prominence of the third eyelid. The sequestrum is a dark brown to black plaque which is oval or round and often raised above the corneal surface. Often clients will describe it as 'a scab on the eye'. Application of fluorescein dye to the cornea often reveals dye retention around the edge of the lesion, but the sequestrum itself does not stain. Sequestra are usually axial (in the center of the cornea), but may be paraxial (off-center). Cats usually develop sequestra on one eye, but bilateral cases occur. The cornea around the sequestrum will be vascularized superficially to varying degrees.

An area of corneal sequestrum surrounded by vascularization and ulceration (arrow).

Are there types of sequestra?

Some cats are present with a faint brown or amber opacity confined to the stroma. Such a patient may not show signs of discomfort. These are thought to be early lesions, lesions following sloughing or surgical removal and subsequent healing, and re-epithelialization of superficial sequestra. These faint sequestra will usually progress, become more dense, acquire distinct borders, separate from the adjacent and underlying stroma and begin the process of ulceration and irritation with loss of the overlying corneal epithelium. The lesion will become larger, darker and deeper. Corneal perforation and globe rupture can and does occur. Some ophthalmologists classify the sequestrum which is darker as a Type I sequestrum, while the lighter brown lesion which is covered by an intact but degenerate epithelium as a Type II lesion. Other ophthalmologists feel that they are both different stages of the same disease process.

What is the treatment for sequestra?

The treatment of corneal sequestrum in the cat varies considerably between veterinary ophthalmologists. Few adopt a conservative approach and allow the sequestrum to slough while treating with antibiotics. Extrusion may take months to years. Waiting is sensible when the lesion is loose and begins to slough. Treatment and ocular pain may be prolonged. The second treatment is surgical excision. The main advantage to surgical excision of sequestra is a significant shortening of the course of the disease (during which the patient is very uncomfortable) and the prevention of the globe rupturing. Superficial sequestra may be treated by superficial keratectomy. The cornea is incised and the lesion removed and the cornea is given support while it heals. Some superficial sequestra may be supported postoperatively with a soft contact lens and third eyelid flap. Sequestra which require deeper dissection may require the placement of a conjunctival or corneal graft for support. Post surgical medical management involves topical antibiotics, possibly anti-viral medications and atropine. An elizabethan collar to prevent self trauma is mandatory. Once the cornea has re-epithelialized, some surgeons recommend the use of topical antiinflammatory medications to reduce fibroplasia and subsequent scarring. Caution is required however, as some cats with sequestrum are positive for feline herpesvirus, and topical steroid may incite reactivation of latent virus. A polymerase chain reaction (PCR) test for feline herpesvirus is recommended for cats with corneal sequestrum.

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Corneal Ulcers

by Dr. Dennis Hacker

What is a corneal ulcer?

An ulcer is a break in the outer surface of tissue. A corneal ulcer is therefore a break in the outer layer of the cornea. Ulcers may occur from a variety of conditions such as scratches by other pets, foreign material such as pieces of grass, sand or dirt getting into the eye, from a lack of tear production and from a failure of the eyelids to remain completely closed during sleep. Uncomplicated ulcers, although painful, should heal in 3 to 10 days (depending on the size) when appropriate treatment is used. Those ulcers that persist are considered complicated.

What types of ulcers are there?

Corneal ulcers fail to heal for two reasons. The first category is comprised of those that fail to heal due to external causes. External causes include: ongoing trauma, unresolved infection, foreign material embedded within the eyelid or in the cornea itself, the failure of the patient to close its eyes fully during sleep, the lack of tear production and abnormally placed eyelashes. These ulcers require treatment of the external cause as well as the ulcer to allow healing to occur. The second category is those ulcers that fail to heal for internal reasons. These are usually primary tissue healing problems or other conditions inside the eye that prevent healing. Primary tissue healing problems refer to conditions at the cellular level in which the cornea itself fails to heal in a normal fashion. This process is recognized in certain breeds, like the Boxer, and older dogs of any breed and are sometimes referred to as a boxer ulcer. Another term for this type of ulcer is indolent ulcer. Other ocular conditions that would prevent corneal healing would be unresolved glaucoma or inflammation within the eye.

How are ulcers diagnosed?

Evaluation of a patient with a corneal ulcer requires a number of diagnostic instruments and techniques. Probably the most important in the evaluation of a corneal ulcer is using the slit lamp-biomicroscope. This instrument permits the veterinary ophthalmologist to carefully evaluate the cornea and ocular structures with a high degree of magnification and resolution. Stains are used to determine the size of the ulcer and if the edges are undermined. Frequently, specimens are obtained for bacterial culture, virus isolation and cytological evaluation.

How are ulcers treated?

Treatment of a non-healing corneal ulcer is dependent on the results of the diagnostic procedures. Ulcers due to external causes require those causes to be treated and, normally, healing rapidly follows. Those that involve other ocular diseases will require those diseases be treated to permit healing of the ulcer. The most frustrating ulcer to treat may be the healing defect ulcer. These ulcers, although generally not sight threatening, take a long time to heal. If healing is prolonged, severe scarring and possible vision loss may occur. Treatment consists of stripping the surface off the cornea and pricking the corneal surface with a needle to Œroughen it. Treatment with antibiotics, medications to dilate the pupil and agents that increase the adherence of the surface to the next layer is then begun. If these therapies do not work a surgical procedure known as a superficial keratectomy is recommended.

What about severe ulcers?

If the ulcer becomes deep, a perforation of the cornea may be the result. These ulcers require aggressive surgical intervention and subsequent medical treatment. Various surgical techniques have been used to treat deep corneal ulcers. The most common procedures used in this clinic are a corneal graft or pedicle conjunctival graft. A corneal graft may be used when the ulcer is along the center of the cornea or in cases of very large, sight-threatening ulcers. The advantage of this procedure is that it provides an immediate seal to the corneal ulcer with a healthy piece of ocular tissue. The graft will scar to some degree, yet vision is possible through the graft. The second technique involves the stitching a piece of conjunctiva (the moveable white tissue of the eye) into the corneal defect. The advantage of this procedure is that it also provides an immediate seal and that it brings healing blood vessels to the area. The tissue remains in place for 4-to-6 weeks. Once healed, the graft may be trimmed after applying a local anesthetic. Corneal ulcers are a frequent problem in veterinary medicine. Your regular veterinarian is equipped to evaluate and manage most of the non-complicated problems. Only those patients with severe or chronic ocular diseases are referred for evaluation to the veterinary ophthalmologist who is specially trained and equipped to treat unusual ocular diseases in pets. Our goal is to help your pet heal and stop hurting.

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Corticosteroid Eye Medication

Inflammation is a frequent and significant part of many eye diseases. The role of inflammation may be relatively mild (as in seasonal allergic conjunctivitis) to severe (as in total eye inflammation with secondary glaucoma).

A wide variety of corticosteroid (cortisone-type) preparations are available to treat eye diseases in humans and our pets. Their general mechanisms of action are a suppression ofinflammation and vascularization, a decrease in pigmentation and a reduction of swelling.

Although the benefits are dramatic and sight saving in many cases, side effects are known to occur. These side effects include: corneal thinning (with extremely long term use), slow healing of corneal injuries and a lowered resistance to infections of the eye. In rare cases, internal side effects have been reported

*If your pet has been placed on topical corticosteroid medication in an effort to control inflammation of the eye or surrounding tissues, your veterinarian has determined this is best to help the eye. The strength of the preparation prescribed has been selected for the circumstances noticed at the time of examination.

If the eye appears to be getting worse, it is important to notify your pet¹s ophthalmologist as soon as possible. Use of corticosteroid medication under the wrong conditions or at the wrong time can lead to irreversible eye damage or blindness.

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Cyclosporine (Optimmune®)

by Renee Kaswan

Optimmune is an ophthalmic preparation of cyclosporine developed and approved for use in animals by Schering Plough Pharmaceuticals Inc. This author began investigating the use of ophthalmically applied cyclosporine in 1983, and discovered its effect on increasing tearing in 1987. The active ingredient in Optimmune, cyclosporine, is a potent immunosuppressive agent developed and approved to prevent rejection of human organ transplants.

The side effects of orally administered cyclosporine can be severe, therefore, the reduction in dose achieved by administering a 0.2% cyclosporine ointment is very important to the safety profile, particularly in small patients. Unlike extemporaneous compounds of cyclosporine used prior to 1995, Optimmune is supplied in a sterile, FDA approved preparation, and Optimmune does not cause ocular irritation. Optimmune has 2 distinct effects on the eye.

• It progressively increases tear production in most dogs. The efficacy of Optimmune in increasing tearing depends on the cause of KCS and the severity. Dogs with very severe dry eye, with a Schirmer tear test (STT) of < 2mm/minute are more refractory to treatment, while 95% of dogs with a STT of >2mm/min will increase tearing with Optimmune therapy. In most patients, an increase in tearing is evident between 2-4 weeks after the start of Optimmune treatment
• Optimmune decreases inflammation in the conjunctiva, cornea and eyelids. This benefit is seen with or without an increase in tearing.

Optimmune can safely be used as a general anti-inflammatory agent to suppress chronic ocular inflammation. Unlike corticosteroids, Optimmune does not inhibit healing of corneal ulcers. Treatment with Optimmune is usually lifelong. In most cases, KCS will relapse if Optimmune is discontinued. The frequency of administration of Optimmune and the requirement for additional palliative treatments may decrease over time, and should be adjusted periodically at re-examination.

Tips for administering Optimmune - If you have not used ophthalmic ointments previously, there are some tricks of the trade to avoid wasting medication. Hold the tube by the crimp when opening, do not squeeze the body of the tube or ointment will propel out too quickly. Use the smallest amount possible per eye.Contrary to the package directions, it is not necessary to use 1/4th inch per eye. Although Optimmune is non-irritative, it is normal for any animal to be fearful of an object coming towards its eyes. If your pet resists treatment, purchase an inexpensive ophthalmic ointment artificial tear product (petrolatum ointment) to use for practice. Approach the dog with the tube behind his head, rather than attempting to charge in toward his anxious wide eyes. As with any behavior, giving a dog treat after administering medication will increase compliance for future treatments.

Owners suffering from dry eye may look forward to a new human product, Restasis. Restasis is in the latest stage of testing by Allergan pharmaceuticals for the treatment of dry eye in human patients.

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How Do I Deal With A Blind Pet?

by Dr. Dennis Hacker

If you woke up tomorrow and couldn't see, you would eventually adjust to being blind and learn where things are in your house. Your pet too will learn where everything is and will adjust to your house and yard if given time. Here are some ideas that will help you and your pet adjust to its blindness sooner.

• Your pet doesn't need to be put to sleep just because it is blind.
• Don't re-arrange your furniture if your pet is mostly indoors. If your pet is an outdoor pet, don't plan major landscape projects!
• If you have a hot tub or pool, a cover or barrier is necessary. Your pet could fall into the water, not find the sides and drown.
• Don't let your pet play in traffic. If you have an outdoor pet and no fence, please check into an "invisible fence".
• If you live in a house or an apartment with a balcony, be sure that your pet cannot walk between the vertical supports and fall to the ground. If necessary, plexiglass should be applied or the vertical supports modified to prevent your pet from getting through.
• Feed your pet and keep its water dish in exactly the same place each and every day. Also, try to have your pet sleep in the same area on a routine basis. These areas will then become reference sites if your pet becomes disoriented.
• If your pet gets disoriented, take him/her to its bed or food bowl. This will be a land mark that will re-orient your pet.
• Put your chair back under the table after meals. Things that are left out will cause your pet to bump and lead to disorientation.
• Until your pet learns about stairs, you will need to place a barrier to prevent him/her from falling down the stairs. The same is true for stair landings.
• Most clients remark that going up and down stairs is the most difficult of all things to "re-learn". Be patient, your pet is trying to do its best.

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Eosinophlic Keratitis

by Dr. Dennis Hacker

What is an "eosinophilic disease"?

An eosinophil is a type of white blood cell. It is seen in all mammalian blood. It is often increased in numbers in patients with allergies and parasitic infections. Cats have several types of dermatologic (skin) eosinophilic diseases: Eosinophilic plaque, eosinophilic or "rodent" ulcer and linear granuloma. The eosinophilic ulcer occurs on the upper lip with the eosinophilic plaque and linear granulomas occurring on the limbs and abdomen. These dermatologic conditions are called the "Eosinophilic Granuloma Complex" or EGC. Over the years, a condition has been recognized which is also unique to cats: Eosinophilic keratitis.

What is eosinophilic keratitis?

In the eye of a patient with eosinophilic keratitis, the conjunctiva (white part of the eye) will initially be reddened initially. Next, a few white "cottage cheese" deposits will develop on the cornea (clear part of the eye) and/or on the conjunctiva immediately adjacent to the cornea. Finally, the cornea will become pink to red and a white plaque will develop on the cornea. If left untreated, the cat can become blind in the eye!

An area of eosinophilic keratitis on the dorsal aspect of the cornea of a cat (arrow).

What causes eosinophilic keratitis?

The cause of eosinophilic keratitis is not known for certain. The cause of EGC is likewise unknown. Eosinophilic keratitis and EGC may be similar diseases due to similar pathologic (biopsy) findings and response to treatment. Pathology results reveal an infiltration of inflammatory cells including lymphocytes, mast cells, plasma cells, eosinophils and histiocytes into the area of biopsy. Over the years, we have noticed several cats with simultaneous infections with herpesvirus and eosinophilic keratitis. In recently published papers, one third of cats with eosinophilic keratitis were positive for feline herpesvirus when corneal and conjunctival scrapings were tested using a viral immunofluorescence test (IFA) and 76% of cats with eosinophilic keratitis were positive using a Polymerase Chain Reaction (PCR) Test for feline herpesvirus.

How is eosinophilic keratitis diagnosed?

Diagnosis of eosinophilic keratitis is by cytological examination of a scraping of the cornea and conjunctiva. Examination reveals eosinophils, neutrophils, lymphocytes and corneal epithelium. Deeper corneal scrapings or pathology sections, obtained by performing surgery, often reveal plasma cells and lymphocytes, with mast cells, eosinophils and histiocytes. In some patients, the scrapings are devoid of eosinophils. In these patients, a different cause is suspected and the term Proliferative Keratitis (PK) has been used. As was stated above, some patients with eosinophilic keratitis also have herpesvirus. It is highly recommended that when collecting a corneal scraping for cytology, that a sample also be collected for a herpesvirus PCR and IFA test. When performed concurrently, these tests are very sensitive indicators of the presence of feline herpesvirus. If these tests are positive, concurrent use of antiviral medications is necessary.

How is eosinophilic keratitis treated?

The first reported case of eosinophilic keratitis was thought to be a corneal neoplasm (cancer). The mass was removed by a superficial lamellar keratectomy. Once the surgical wound had healed, the eye was treated with subconjunctival and topical steroids. When the medication was stopped, the condition returned. Due to similarities between the pathology findings of this case of eosinophilic keratitis and the eosinophilic granuloma complex, veterinary ophthalmologists used a birth control medication, megestrol acetate (Ovaban, Schering), for the treatment of the recurrence of the condition in this cat with excellent results. The dosage used was 5 mg daily for 30 days, at which time the dosage was reduced to 5 mg every other day. Other authors reported varying dosage regimes of megestrol acetate which would provide clinical remission. The 5 mg daily or every other day is an extremely high dosage and can lead the cat to develop diabetes mellitus or other side effects such as increased appetite and weight gain, behavior change, mammary gland enlargement and adrenal gland suppression. These side effects are similar to those caused by steroids in cats. Because of these side effects, Dr. Hacker recommends that megestrol acetate be used at much lower doses when appropriate. Alternatively, topical antiinflammatory therapy may be used. Most patients with eosinophilic keratitis respond when topical dexamethasone or prednisolone acetate is applied 2-to-3 times daily. Treatment frequency is reduced as the patient responds to the medication. When accurately diagnosed and treated, eosinophilic keratitis is a readily controlled disease. It may require lifelong treatment for the kitty. Each case is different.

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Eyelid Abnormalities

by Dr. Dennis Hacker

Common problems of cats & dogs

UPPER AND LOWER EYELID

The upper and lower eyelids have many functions. They protect the cornea [clear portion out front of the eye] and the eye itself from drying out, from insults and trauma from the outside. They spread the tears (tear film) across the cornea. They produce portions of the tear film from glands along the eyelid margin and from cells in the folds of the eyelids. They determine the shape and size of the eyelid openings. They keep out the light. Finally they pump the tears out to the tear duct. Meanwhile, the third eyelid helps to spread the tear film and produces from 30-to-60 % of the watery portion of the tears. The eyelids of dogs and cats open between 10 and 14 days of age. If the eyelids open too early, tear production is not present and signs of dry eye (keratoconjunctivitis sicca) will occur unless you apply antibiotic ointment 3-to-4 times daily until tear production begins. A condition known as conjunctivitis neonatorum occurs when bacteria or viruses enter the eye through the eyelids that are closed following birth in dogs and cats. Corneal rupture and chronic scarring of the cornea and the white of the eye (conjunctiva) will occur unless the eyelids are opened by a veterinarian and the eyes are treated with appropriate medication.

We now know that in kittens, conjunctivitis neonatorum is due to herpesvirus infection. These kitties will benefit from appropriate antiviral medication. Cortisone medication should not be used in these patients. A lack of portions of the eyelid occurs in cats and is known as eyelid agenesis oreyelid coloboma. This condition is seen in the lateral portion of the upper eyelid. This condition will lead to scarring and blood vessels occurring in the cornea because tears are not spread normally and because hairs on the 'eyebrow' will rub the cornea. Surgery is necessary to correct this condition. An abnormality known as dermoids can occur along the conjunctiva (white of the eye) on the upper eyelid or along the lateral eyelid opening.

Dermoids are normal skin tissue at an abnormal spot. Depending on the size and location, these growths may be left alone [if they are causing no problems] or removed during surgery. Eyelash disease is actually a group of conditions that cause eye injury from hairs that irritate the eye. Trichiasis is a condition of normal hairs lying on or irritating the globe. Examples of this would be very long facial hairs in long haired dogs and nasal folds in the Pekingese. Also tiny hairs at the nose side of the eye can act as a wick and cause tear spilling in Miniature Poodles and Persian cats. Distichiasis is the condition of an eyelash coming out of an abnormal position in the glands that are located along the eyelid edge. Districhiasis is more than 1 eyelash coming out of each of the gland openings. Ectopic cilia are abnormal hairs that exit a hair follicle on the inside of the eyelid. Ectopic cilia are very painful. The successful elimination of the offending hairs will require surgical freezing.

Excessive facial folds are seen in the newborn Shar Pei at the time of eyelid opening. The most common treatment is the use of 'temporary tacking' using either sutures or staples to hold the eyelids away from the cornea to prevent damage. Lagophthalmos means 'rabbit eye' and is commonly seen in the Pekingese, Pug, Boston terrier, Lhasa Apso, Japanese Chin, Dandy Dinmont and Shih Tzu, and the Persian, Burmese, Exotic Shorthair and Himalayan breeds of cat. Whilst these animals may not exhibit any signs of eye problems for years, increased pigmentation will start on the cornea at the nose side of the eye. An all too common presentation will be the patient that develops a corneal ulcer in the center of the eye. Lagophthalmos usually requires surgery to prevent further damage that can cause the eye to rupture.

Entropion (rolling in of the eyelids) and ectropion (rolling out of the eyelids) are conditions caused by abnormal eyelid position in relation to the globe itself. If the patient has heavy facial features, they will probably have ectropion. Only if it causes exposure problems will ectropion need correction. If the eye size is relatively small for the size of the orbit, entropion will result. Entropion will often cause abrasions of the cornea and/or irritation of the conjunctiva. This is very painful and almost always requires surgery to correct. Entropion or ectropion may occur due to scarring from previous injury or surgery.

Acquired conditions include: Eyelid neoplasm. Research has shown that in dogs, approximately 75% are benign (do not spread). That does mean that 25% are malignant (do spread) and therefore, all removed masses should be submitted for pathologic examination. In cats, the ratio of benign to malignant tumors is exactly reversed so that 75% are malignant. Chalazia are firm, swollen masses that are well localized. They are removed surgically and pathology should rule-out the possibility of neoplasm. Eyelid lacerations are injuries that should be sutured as soon as the patient's stability permits. Facial nerve palsy (paralysis of eyelids) is commonly seen in patients with chronic ear infections [American Cocker Spaniels]. Because of the paralysis of the muscle that circles the eye, the eyelids cannot blink and the cornea will dry out due to an uneven spreading of the tears. This drying can lead to ulcers, infection and even globe rupture. Medication alone may help although surgery may be needed to save the eye! Eyelid inflammation is known as blepharitis. This is often seen as enlargements of the glands of the eyelids that will appear as small abscesses on the globe surface of the eyelid. Gland contents may be expressed by the ophthalmologist and the contents cultured. Treatment will involve broad-spectrum antibiotics and cortisone given by mouth, topically applied antibiotics and warm, moist compresses.

THIRD EYELID OR 'HAW'

The gland of the third eyelid may become everted. The exposure to the air will cause the gland to become red and the condition is called cherry eye. Because the gland produces 30-to-60% of the tears, it should not be removed. Surgery should be performed to replace the gland and thus preserve its function. Occasionally in young patients, the third eyelid will become folded causing a 'funny' look to the eye (everted third eyelid). This folding often leads to excessive tearing. This eversion is irritating to the patient and should be corrected surgically. As with the eyelids, lacerations and neoplasms may occur to the third eyelid. They should be treated the same as similar conditions of the upper and lower eyelids. Eyelid conditions are often irritating to our pets. With proper treatment, surgery and medication, further worsening of the condition can be prevented.

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Glaucoma

by Dr. Dennis Hacker

What is glaucoma?

Glaucoma is the elevation of pressure inside the eye (intraocular pressure) beyond a specific point at which vision is no longer possible. Glaucoma is a frequent cause of blindness in humans and in our pets. To understand glaucoma, it is necessary to understand how the fluid inside the eye normally flows and maintains normal intraocular pressure.

Fluid inside the eye (aqueous humor) is produced behind the colored area of the eye (iris) in a portion of the eye called the ciliary body. This aqueous humor is made by filtering blood. The fluid flows through the dark hole in the eye (pupil). Finally the aqueous humor drains from the eye at the junction of the clear cornea and the colored iris (drainage angle) inside the eye and then the aqueous rejoins the blood. The drainage angle is a sieve-like network. This aqueous humor is made inside the eye and passes from the eye at the same rate. This results in a stable intraocular pressure of 15-25 mm of Hg. Glaucoma is the consequence of a blockage of the outflow of aqueous humor and a subsequent buildup of pressure inside the eye.

The resulting high pressure compresses the optic nerve and results in pain and in blindness. Are there types of glaucoma? There are two categories of glaucoma. Primary glaucoma occurs without any obvious disease in the eye. Secondary glaucoma occurs when some other cause is present. Another way to categorize glaucoma is based on how the drainage angle appears on examination. The drainage angle may be open, narrowed, closed, or abnormally developed.

Primary glaucoma is known to occur in certain purebred breeds of dogs and is thought to be inherited. Breeds in which we see primary open-angle glaucoma are the Beagles, Miniature Poodles and Norwegian Elkhounds. Narrow-angle glaucoma (an abnormal narrowing of the outflow channel) is seen in American and English Cocker Spaniels. In a developmental abnormality of the drainage angle (goniodysgenesis) the outflow is decreased during times of inflammation. This condition is commonly seen in the Basset Hound, American and English Cocker Spaniel, Samoyed, Flat-coated Retriever and Chow Chow.

Secondary glaucoma is the result of some intraocular condition that interferes with the natural flow of aqueous humor. Conditions that commonly cause secondary glaucoma include the result of ocular inflammation (uveitis), lens dislocation (luxation), neoplasm (cancer), previous surgery and injury to the eye. Glaucoma results in blindness by blocking the nerve impulse through the optic nerve. Once the optic nerve has been permanently damaged, there can be no restoration of vision. With early surgery and then medical therapy, your pet's vision may be maintained. Frequently with extreme elevations of pressure, the eye becomes permanently blind and painful very rapidly.

The aim of therapy at that point is to keep your pet pain-free and maintain a cosmetic eye. How is glaucoma diagnosed? The diagnosis of glaucoma is based on history, clinical signs, measuring the intraocular pressure [tonometry] and visually examining the drainage angle using a process known as gonioscopy. We cannot use the signs of "pain" as a criteria as our pets cannot tell us of their pain directly. Clinical signs of glaucoma include some or all the following: excessive tearing, a green or yellow eye discharge, a reddened eye, an eye that suddenly looks blue, an eye with a pupil that is large and will not move when light is shined into it, a pet who sleeps a lot, a pet who hides under the bed or a pet who suddenly becomes frightened or irritable.

People with glaucoma often report a constant headache that medication will not help. An eye with glaucoma becomes enlarged in later stages of the disease. Tonometry is the measurement of pressure within the eye. A variety of techniques can be used to estimate intraocular pressure, including SchiÖtz tonometry and applanation tonometry. In our clinic, we use the highly accurate applanation tonometer. Gonioscopy is a technique used to evaluate the drainage angle. It involves placing a dome-shaped contact lens [goniolens] on the corneal surface after numbing the eye with topically applied anesthetics. This lens allows us to directly visualize the drainage angle. Gonioscopy occasionally requires sedation but in most pets it can be performed after the use of topical anesthetic only. The technique is essential to evaluate the eye that doesn¹t have glaucoma for risk of a future problem.

How is glaucoma treated?

Many of us have friends or relatives who have glaucoma. They simply place drops in their eyes several times a day and have very few problems that result in vision loss. In some people medication will not resolve the glaucoma and surgery is necessary. This is what we face in animals all the time and this is what makes glaucoma very difficult to treat in domestic animals.

After the initial diagnosis of glaucoma is made, your pet is aggressively treated with medication if there is any hope of saving vision. This will require a period of hospitalization. During periods of hospitalization, medication (mannitol and Diamox®) may be given directly into the vein to help reduce the intraocular pressure. Additional drugs are used that are aimed at increasing the outflow of aqueous humor and/or suppressing its production. These drugs may include pilocarpine, Trusopt®, timolol, Betoptic®, epinephrine, newer synthetic epinephrine-like drops and combinations of these drugs. Topically applied prostaglandins, such as lantaprost, also have been used in humans to reduce intraocular pressure.

Yet more medications, known as carbonic anhydrase inhibitors, are aimed at reducing the production of aqueous humor. Examples of these medications are Daranide® and Neptazane®. Once the pressure has been controlled, surgery is essential to maintain vision. It is impossible to control glaucoma with medication alone in dogs, cats and horses! A variety of surgical techniques have been developed to aid in the control glaucoma.

NEWS! NEWS! NEWS!

At the most recent A.C.V.O. (American College of Veterinary Ophthalmologists) meeting in Seattle, WA, Dr. Dennis Brooks from the University of Florida, an internationally known expert on glaucoma in animals, reported that calcium channel blocking drugs may help prevent damage to the optic nerve in patients with glaucoma. Such drugs as Norvasc® may thus help prevent damage to the retina and optic nerve and should therefor be given to pets with glaucoma.

If my pet has glaucoma and can still see, what can be done?

Laser surgery is the treatment of choice in pets with primary glaucoma who can still see. As with the freezing procedure listed below, no cutting is required. Your pet does have to be anesthetized so he or she won¹t move. The laser burns completely through the white outer layer of the eye without damaging it except for redness and swelling.

The laser selectively kills small areas of the ciliary body and this reduces fluid production. The main complication of this technique is that it is like the Marshall of an old west movie who is shooting through the wall of a building to try to kill the villain. He can't see the villain and similarly the Doctor cannot see the ciliary body. Occasionally the ciliary body will not be damaged enough and a second procedure is needed to lower fluid production and restore normal intraocular pressure. Another complication is that the intraocular pressure may actually increase in about 5-10% of patients due to an initial increase in fluid production. This complication usually occurs in patients who have had previous glaucoma "episodes." The elevation of intraocular pressure will require a filtering "shunt" be placed to draw off excessive fluid.

If a pet has glaucoma secondary to the loosening and dislocation of the lens (luxation), the lens must be removed to resolve the glaucoma. Laser cycloablation surgery may be needed at the time of the original surgery or during a second surgery to permanently control glaucoma. This procedure is also recommended as a preventative in the second eye of pets who have glaucoma and are blind in one eye and are currently visual in the second eye.

Cyclocryothermy (cryosurgery) is a freezing procedure that was developed a number of years ago to decrease the production of intraocular fluid in the eyes of pets who can still see. The technique involves freezing the ciliary body with a small probe placed on the outside of the eye. No cutting is required. Again, your pet will have to be anesthetized to prevent them from moving. The freezing kills the cells in the ciliary body that produce the aqueous humor. A number of sites are frozen depending on how elevated the pressure is. After surgery, there is considerable swelling and redness to the white of the eye that is to be expected.

Complications of this technique include retinal detachments, severe intraocular inflammation, high intraocular pressure immediately following the freezing that may lead to permanent blindness, shrinkage of the eye or cataract formation. As with the laser surgery, if cryosurgery is performed and the intraocular pressure increases, a filtering "shunt" may be needed to reduce the pressure. Finally, the glaucoma may return at a later date requiring a second surgery. A new development for patients with glaucoma is the injection of cidofovir (Vistide®) into the back of the eye to damage the ciliary body and reduce the intraocular pressure. Vistide® was developed for use in humans with cytomegalovirus retinitis. A side-effect was the pronounced reduction of the intraocular pressure. By 'titering' the dose, we hope to reduce the intraocular pressure in dogs. Complications of this procedure are intravitreal hemorrhage, retinal detachment and return of the glaucoma requiring repeated injections. Although the injection of Vistide® is a recent therapeutic development, success rates vary from only 10-25 % of patients being helped depending on the cause of the glaucoma.

Only time will tell if the reduction in intraocular pressure is permanent or temporary. The nice thing is that this procedure can be repeated as needed. What if my pet cannot see any longer? The goal of surgery in this situation is to help make your pet pain free. One technique employed to result in a cosmetic, pain-free eye for your pet is the placing of a silicone implant inside the eye [intraocular prosthesis]. The technique involves removal of the contents from the inside of the eye--leaving the outer shell of the eye--and implanting a silicone implant within the wall of the eye. The shape of the eye is maintained and the eye moves normally. If you think of making a 'forever' grape by scooping out the insides and placing a marble within the grape skin and finally sewing the skin of the grape closed, you have some idea of how the surgery works. Following the initial postoperative treatment, minimal care is needed and the eye is maintained in a relatively normal cosmetic appearance while being pain-free.

Complications of this technique are that corneal ulceration occasionally occurs following surgery (due to drying) and scarring of the cornea (resulting in a gray appearance.) Another technique used to control glaucoma is the injection of antibiotic compounds into the inside of the eye. These antibiotics in high concentrations result in a killing effect on the ciliary body resulting in the reduction or cessation of the aqueous humor production. If the eye was visual the antibiotic would also kill the retina resulting in permanent blindness. Therefore, this technique can be used only on eyes that are definitely blind due to chronic pressure elevations. Your pet will have to be sedated and an anesthetic is applied to the eye and injected immediately beneath the white conjunctiva. Complications of this technique are generalized shrinking of the eye, return of the glaucoma at a later time, blindness if the eye was visual and occasionally chronic pain. This technique is only of value in quite elderly pets or pets who cannot safely undergo anesthesia for medical reasons such as kidney failure. Another therapeutic modality is injection of Vistide® as stated above. Finally, the blind, painful eye may be removed (enucleated). After the eye is removed, the skin is stitched shut and the hair will re-grow over the surgery site and a slight amount of pigment will be left. This surgery again requires that your pet be anesthetized. The possible complication to this technique is possible infection.

What is the long term chances for my pet?

Glaucoma is seldom diagnosed early enough to restore vision in the first eye affected. Therefore, during the initial examination time will be spent to evaluate the "good" eye. Eventual outcome depends upon early accurate diagnosis, possible laser preventative surgery, appropriate medical therapy, and regular and consistent reevaluations to save the vision of the remaining eye.

Conclusion

Glaucoma remains a leading cause of blindness in veterinary patients. Because of the nature of the disease, many pets are presented at a time when it is not possible to restore vision to the first eye affected. Glaucoma is very difficult to treat in our pets. Unlike humans where medication resolves over 80% of the cases of glaucoma, surgery is almost always required in veterinary patients. The goal of the Veterinary Ophthalmologist in treating a pet with glaucoma is to restore vision when possible and, if vision is not possible, to help your pet remain pain-free. Additionally, we want to maintain vision in the second eye as long as possible. Your Veterinary Ophthalmologist teamed with your regular Veterinarian will recommend appropriate therapies suitable for your pet and your circumstances.

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Feline Herpesvirus Infections

by Dr. Dennis Hacker

One of the more common ophthalmic problems seen in our cat patients is infections caused by herpesvirus. This virus causes conjunctivitis (inflammation of the moveable white tissue surrounding the eye) and/or corneal ulcers. Occasionally sneezing and mouth ulcers occur in some patients. We hope this paper will give you information concerning this common condition.

WHAT DOES A VIRUS DO?

A virus is not alive in the sense that you, I, your cat and even bacteria are alive. A virus is a capsule that contains only protein or nucleic acids known as DNA. This DNA is the building block that makes all of us who and what we are. As it is not alive, a virus particle cannot reproduce without a living cell to which it is able to attach itself. Once attached to a susceptible cell (a cell that will support the virus growth), the viral DNA (vDNA) is injected into the cell. The vDNA then continues to the cell nucleus that is the 'control center' of the cell. The vDNA then inserts itself into the cell's DNA. This causes the cell to start manufacturing new virus particles. To do this, the cell takes nucleic acids and proteins from the area surrounding itself and uses them to form new vDNA. This concept is important in how we must treat viruses that we will see below.

WHAT IS HERPESVIRUS?

Feline herpesvirus is specific to cats. There are also dog herpesvirus, people herpesvirus, cow herpesvirus, chicken herpesvirus and horse herpesvirus. In fact, most animals have their own type of herpesvirus. These viruses will not infect other species, i.e., when a cat has herpesvirus, the owner has nothing to fear as far as getting the disease. Herpesvirus is a common respiratory pathogen (infectious agent) that causes an upper respiratory disease in most cats. The virus is everywhere and it infects most cats in almost every cattery in the country. It is our belief that almost every kitten is exposed to this virus following birth as the virus is often found in the birth canal of the queen. As a respiratory disease, the virus is acquired by aerosol, that is one cat sneezing around another cat. The virus is killed by drying and sunlight but can live for many hours in a moist, cool environment.

The problems associated with herpesvirus depend on the age at which the cat first acquires the virus. Neonatal conjunctivitis occurs in kittens who have not yet opened their eyes.

A young kitten with neonatal conjunctivitis. The arrow indicates an infection which had developed behind closed eyelids.

Herpesvirus conjunctivitis in a juvenile kitten

possible corneal ulcers (erosions) ay occur.

In older patients, conjunctivitis is most often seen. Sneezing may or may not be seen in any of these patients. Most often, our patients have had a long-standing history of conjunctivitis and/or corneal ulcers that will not heal. We have seen cats who have had herpesvirus infections for as long as 12 years! When herpesvirus invades nerve tissues, a possibility of relapse exists. Perhaps only 15-to-20% of the cats with herpesvirus infections have relapses, yet this possibility must be kept in mind.

As many of my clients know, human herpesvirus may cause the skin conditions known as 'cold sores' and 'shingles.' As with 'cold sores' and 'shingles,' any stressful episode may cause a recurrence of the infection. In cats, a relapse may be triggered by the owner leaving town and a stranger coming in to feed the cats, being boarded, or strangers or new animals coming for a visit. We have one patient that has a new episode of herpesvirus every time the client leaves town for a business trip. Knowing this helps us understand the recurrence of redness following a stressful episode. This redness indicates a probable return of the herpesvirus infection and requires re-institution of the medication. Again, these relapses do not occur commonly.

HOW DO YOU DIAGNOSE HERPESVIRUS?

Herpesvirus infection should be suspected anytime a cat has an eye problem that does not respond to antibiotics (which have no effect on viruses). To diagnose a herpesvirus infection, after applying a topical anesthetic, a scraping of cells is made from the eye and placed on a slide. The slide is submitted to a laboratory for a specific test procedure known as an Polimerase Chain Reaction (PCR) test. This test is quite specific when compared to other tests. A different staining test can be performed which is known as the Indirect Flourescent Antibody Test (IFA). While the IFA test is not as precise as the PCR test, performing both tests simultaneously gives a better infection indicator as to whether your cat does or doesn't have herpes than either test alone. Another test that can be used is virus isolation that actually grows the virus in tissue cultures. This test takes up to 1 month and is quite costly.

HOW DO YOU TREAT HERPESVIRUS?

If you or your child has a bacterial infection, a strep throat for example, penicillin may be given and the penicillin will kill the strep organism and the infection will go away. This is because the bacteria are alive and reproducing all the time. As mentioned earlier, a virus is active only when it gets into a cell. This is why antibiotics do not kill viruses. Since the living cells must bring in nucleic acids and proteins (protein building blocks) from the local cellular environment to make new viruses, the only way to kill susceptible viruses is to put abnormal proteins and nucleic acids in the environment. This is the way herpesvirus is killed.

We use medications such as Herplex®, Viroptic®, or Vira-A® to introduce abnormal proteins into the environment. The infected cells draw these proteins into itself and use them to make new virus particles. These virus particles will then not be able to reproduce. Because we do not know how long it takes to kill all the virus particles this way, treatment must be continued for 4-to-6 weeks or longer! Occasionally, patients need to be treated longer' Herpesvirus can become resistant to these medications. This does not happen often, yet this fact should be kept in mind, especially if a patient initially improves and then relapses. If resistance occurs to one medication, a change to another medication can be made. If resistance occurs to all the commercial eye medications, an oral drug called Zovirax® (acyclovir) may be prescribed. This drug appears to work well in humans and rabbits, yet the full spectrum of its side-effects is not known in the cat. This drug is reserved for the most resistant cases.

Eye medications must be applied often. This means 5 times a day! For clients who do not work or working clients on weekends, the medication is applied every 3 hours for 5 treatments. During the week for clients who work, I recommend treating when you awaken, before leaving for work, when you get home, half-way between arriving home and bedtime, and bedtime. This is 5 times a day although they are not equally spaced. One other aspect of these anti-herpes medications should be kept in mind. That is that any protein has the ability to cause an allergic response! You may know of someone who wears soft contact lenses. If they fail to clean the lenses to remove their body proteins, an allergic reaction occurs which may be quite irritating. As stated above, you are applying abnormal proteins directly into the eye of your pet. If you notice the eye and eyelid becoming quite red, you must call us immediately.

Due to the possibility of the allergic response and the virus becoming resistant to the medication, re-examinations are critical. In addition to the medication previously discussed, we will probably dispense two others: Interferon and lysine. Interferon is a natural chemical produced by the body to fight off viruses. The application of this to the eyes five times daily induces the patient to produce more of their own interferon. We have also found that after the active infection is controlled, the use of interferon even once a day seems to help prevent relapses! Finally,lysine has been shown to help kill herpesvirus. Lysine is very safe in cats. If it is possible to give your pet tablets by mouth, lysine has been a definite help in cats with herpesvirus infections.

If all three medications are prescribed for your pet, you will be using Herplex® (idoxuridine), interferon and lysine. The idoxuridine is applied to the eye(s) five times daily as stated above. Interferon is applied to the eyes five times daily and one minute after the idoxuridine. Lysine is given by mouth twice daily and may be mixed with food although the best way to give it is to simply pop it down the mouth. Although herpesvirus infections are treatable, the infections can be frustrating because not every cat can be treated the same as all others. Sometimes medication must be changed to provide results. Patience from everyone, you, your cat and your ophthalmologist is required.

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Horner's Syndrome

by Dr. Dennis Hacker

Horner's syndrome is an intriguing disorder of the nervous system that is complex to explain. There are two major divisions of the nervous system. There is the part of your nervous system that you are aware of and have control over. For example you feel cold and in response you consciously initiate all the actions that result in you putting on a jacket. This is the voluntary nervous system. Additionally there is the part of your nervous system that is under automatic control. You cannot control this system and the actions occur without your input. Again you feel cold and start to shiver. That occurs without your control or input. Similarly, you do not have to think to make your heart beat. The automatic (doctor's call it autonomic) nervous system - the part you have no control of - itself has two divisions... the sympathetic and parasympathetic nervous systems.

If you have just finished a large meal and are sitting around feeling "stuffed" and feel "snoozy" you are feeling the actions of the parasympathetic nervous system. During this time, your pupils will be small due to constriction. If someone attacks you with a knife, your pupils dilate, blood is shifted to your muscles and your heart beats faster. This is the 'fight or flight' reaction and is characteristic of the sympathetic nervous system. The eye, and the rest of the body as well, receives both sympathetic and parasympathetic innervation. Under normal conditions there is a fine balance between sympathetic and parasympathetic stimulation. If something were to block the sympathetic impulses into the eye, there would be an over balance of parasympathetic supply to the eye. This is what happens in Horner's syndrome.

On its journey to the eye, the sympathetic nerve begins in the brain, travels down the spinal cord to the shoulders and exits from the spinal cord. After exiting, the sympathetic nerve joins an artery and vein and travels back toward the head. At the base of the ear, a nerve junction (ganglion) occurs. The portion of the nerve from the brain to the shoulders and back to the base of the ear is called the pre-ganglionic nerve. After the ganglion, the nerve goes to the eye. This is the post-ganglionic nerve. Around the eye are several muscles responsible for moving the eye which are under voluntary control. Surrounding these muscles is a smooth muscle cone which is controlled by the sympathetic nerve. The nerve causes the smooth muscle cone to become constricted and this in turn pushes the eye slightly forward to its normal position in the orbit. If the sympathetic nerve is not working well, the eye will sink somewhat into the orbit.

When this occurs the inner or third eyelid will become prominent and the upper eyelid will become droopy. The sympathetic nerves surround blood vessels within the conjunctiva (white portion of the eye which we see) and cause an ever so slight constriction of these vessels. With the loss of the sympathetic nerves, these conjunctival blood vessels dilate and the conjunctiva therefore looks more red. Surrounding the pupil a sphincter (closing) muscle is present which is under parasympathetic control. Working against the sphincter muscle are radially arranged dilator muscles very much like spokes on a bicycle. These dilator muscles are under sympathetic control. If the sympathetic nerve is not working well, the pupil will be smaller than normal because the dilator muscles cannot work against the sphincter muscle.

All the above describe Horner's syndrome. Horner's syndrome is associated with damage to the sympathetic innervation to the eye. The damage may have numerous causes and may occur anywhere along the course of the nerve's route from the brain to the eye. Thus Horner's syndrome may be associated with anything from brain tumors; spinal cord injury in the neck; thoracic tumors such as lymphosarcoma or thyroid tumors; injuries to the neck from fighting or trying to draw blood; middle ear infections; and nerve abnormalities caused by viral, immune-mediated or other causes.

Of all dogs diagnosed with Horner's syndrome 80% or more will be middle aged to older Golden Retrievers. Cocker Spaniels are the second most commonly affected breed because of chronic ear infections. Most cases of Horner's syndrome are idiopathic (of unknown cause) and spontaneously recover within an average of 16 weeks. A thorough physical examination is warranted to determine if any of the causes of Horner's syndrome are present. Blood tests and chest radiographs (x-rays) may be needed. A pharmacologic test should be performed by the veterinary ophthalmologists to further localize the site of the nerve abnormality, that is pre-or post-ganglionic Horner's syndrome.

If Horner's syndrome is suspected to be due to unknown causes, only time will resolve the condition IF it can be resolved. The symptoms however may be reversed temporarily by the use of eye drops two or three times daily. Because the eyedrops lose effectiveness with continued use, they will have to be used more and more frequently. Thus, unless the patient is a show pet and drops can be used while they are in the show ring, drops are not effective for the long run. It is important to know that your pet is not in pain. The eye conditions are due to a nerve problem which is not painful. It just looks 'abnormal.'

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Iris Melanoma

by Dr. Dennis Hacker

What is a melanoma?

A localized area of increased pigmentation is called an iris melanoma. This term means a tumor or growth of pigmented (melanin-containing) tissue. These are seen mostly frequently in cats, especially older cats, and less frequently in dogs. These are also known as "iris nevus", "iris freckle" and "melanosis." Melanosis just means pigmentation of tissue.

Where are they located?

These tumors are located on or within the iris. The iris is the colored portion of the eye which we see when we look at each other and at our pets. These lesions are most commonly seen in cats due to the iris color which is common in cats. In dogs, the iris is usually light to medium brown. In cats, the iris is either gold, yellow, blue or green. For this reason, a brown growth is seen earlier in cats.

What do these 'melanomas' look like?

Melanomas of the iris can look like single or multiple flat dark spots (called iris nevus if singular or nevi if multiple), or as if the color of the entire iris has changed to a dark brown.

The black arrow indicates an early darkening of the iris in this cat. An early pigmented iris lesion (iris melanoma) is present.

The white arrow indicates a more diffuse pigmented iris lesion (iris melanoma).

More numerous pigmented iris lesions in this cat. Alternatively, there may be single or multiple dark, raised masses of the iris.

The dark arrow indicates a raised, dark tumor of the iris (iris melanoma). This eye was removed and the pathological diagnosis was a malignant lesion.

What do you mean they're not always correct?

Just that! Understand, just by looking at the lesion of the iris, NO ONE can tell exactly what a lesion is. Removing the eye or the lesion and performing pathology is the only way to know for sure what a lesion is. A pathologist can determine what a tissue is by microscopic examination of tiny pieces of the mass. When a Veterinary Ophthalmologist examines a patient using a slit-lamp biomicroscope, we can see what the lesion looks like grossly. Based on the experience of the Ophthalmologist, an educated guess can be made. Without removing the lesion, no one will know exactly what it is. There are techniques of using a syringe and small needle to "vacuum" cells off the lesion in an attempt to make a diagnosis. Unfortunately, within any tumor, cell types vary and what is on the surface of the iris isn¹t always what¹s down deep inside the mass.

What should be done with an iris melanoma in my pet?

What should be done for any one individual patient should be based upon the age of the pet, the overall health of the pet, any intraocular (within the eye) complications and the extent of the tumor. Currently a controversy exists in veterinary ophthalmology about the best way to deal with these lesions. Veterinary pathologists who deal primarily with ophthalmic tissue examination recommend that ANY iris melanoma lesion should be cause for removal of the eye. Their rationale for this is that they have seen numerous cases where the tumors have spread (metastasized) outside the eye. In several cases, the patients have died from the tumor spreading through the body.

Many Veterinary Ophthalmologists have seen patients, especially cats, who have had these lesions for years and eventually died from other causes, such as kidney failure. Because of these cases, most but not all Veterinary Ophthalmologists recommend when the patient has diffuse melanosis of the iris only observation be performed on a semi-annual basis. Once signs of glaucoma or uveitis occurs, then enucleation be performed because to these conditions. Alternatively, if the lesion is solitary, it is possible to either open the eye and remove the melanosis and submit it for the pathologist to examine or to use a laser to destroy the tumor. The advantage of the surgical removal of the melanosis is that you can determine the exact type of tumor it is. The disadvantage of this is that the eye must be opened, bleeding can and will usually occur and it is only feasible to perform on small lesions.

The advantage of the laser procedure is that the eye doesn't have to be opened, it can be repeated to remove additional tumors or repeat on the original tumor and that the postoperative period and treatment is much less than with the surgical procedure.

The disadvantage of the lasering is that the type of tumor cannot be determined for certain. BUT, if the tumor is gone, and it is early in the course of the condition, then the type of tumor isn't really as important as it might be if the tumor is large.

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Keratoconjunctivitis Sicca or Dry Eye

WHAT IS DRY EYE?

Keratoconjunctivitis sicca (KCS) or "dry eye" describes the changes in the eye which result from lack of tear production. To understand dry eye, it is helpful to know how tears help keep the cornea healthy. The cornea is the clear portion in front of the eye. Like all living tissue, the cornea requires a supply of oxygen and food for energy to remain healthy. Oxygen and food are supplied to most tissue by the blood that moves through the area. The healthy cornea has no blood vessel so the oxygen and food are supplied through the three layered 'tear film.' The outer most layer of the tear film is an oily layer supplied by glands in the eyelids. This layer helps prevent evaporation of the next layer. The middle layer is the liquid (watery) layer produced by the main tear gland and a gland in the third eyelid. This is the layer where the decrease in tear production takes place. The innermost layer in direct contact with the cornea is a layer of mucous produced by glands located in the folds of the eyelid. The mucus layer helps the water layer remain attached to the cornea. A breakdown of the tear film by a loss of the water layer causes dry eye. This loss results in dryness to areas of the corneal surface or, in more advanced cases, drying to the entire corneal surface.

When the cornea is deprived of oxygen and food through the tear film, it rapidly undergoes destructive changes. These changes result in brown pigmentation, scar tissue growth, blood vessel growth and even ulcer development. These changes may lead to partial vision loss. The eyes of a patient with KCS sting constantly just as ours do on a very windy day. The stinging we feel is due to the wind drying our eyes quicker than tears can be provided. Therefore, the patient with dry eye is uncomfortable almost all the time.

When a patient has dry eye, or a lack of the watery layer of the tears, the oil and mucus layer production is relatively increased. This leads to a thick, gunky, greenish discharge that sticks to the hairs around the eye. Often this is the main reason that a patient is presented to the Veterinarian. The discharge will clear up when medication is used frequently enough but the discharge will return when the medication is stopped. When this occurs, the patient is often referred to a Veterinary Ophthalmologist for further examination and treatment.

This is what a typical patient with KCS looks like.

DIAGNOSIS OF KERATOCONJUNCTIVITIS SICCA

Diagnosis is made by determining how long the condition has been on-going, what the doctor sees when the patient is examined and a number of testing procedures. These tests include the Schirmer tear test that measures how much of the watery layer is produced in one minute.

Fluorescein stain (a bright green stain) is used to define possible breaks in the corneal surface and the rate of the tear breakup. In addition, Rose Bengal stain (a reddish pink stain) may be used to evaluate the health of the outer layer of the cornea called the epithelium. Examination of cells is sometimes recommended to define the state of health of the conjunctiva. This test has both a prognostic and therapeutic value.

WHAT ARE THE CAUSES OF KERATOCONJUNCTIVITIS SICCA?

A number of causes have been reported for dry eye. These include hypothyroidism, infections of the tear glands such as canine distemper virus and immune mediated diseases that attack the tear glands. Loss of nerve impulses to the gland due to longstanding ear infections will cause dry eye in some cases. Another frequent cause of dry eye is a toxic effect produced by some sulfa-containing drugs. Some of these drugs may have been given for the treatment of other diseases. It may not be possible to change the patient's medications and occasionally dry eye is treated despite being caused by other drugs. In many cases the cause of dry eye remains unknown yet treatment can still be instituted.

WHAT IS THE TREATMENT OF KERATOCONJUNCTIVITIS SICCA?

There are several considerations in treating dry eye. A prime consideration is to reduce the overgrowth of bacteria that is common in the dry eye syndrome. The dry eye patient frequently has a buildup of mucus in the folds of the eyelids that are no longer being washed with liquid tears. This mucus is food for bacterial growth. These bacteria may not be disease causing bacteria but need to be controlled.

Topical antiinflammatory drugs are indicated when green stain shows no ulceration. This medication reduces inflammation and long term scarring effects. Corticosteroids (cortisone drugs) cannot be used when ulcers are present because they decrease healing speed and enhance the ulcer process. Along with antibiotics and cortisone drugs, artificial tear ointments are sometimes used to provide prolonged corneal contact overnight and during times that the patient cannot be treated frequently.

Occasionally patients with a nerve loss are treated with pilocarpine given by mouth. This drug stimulates the tear gland. Unfortunately, pilocarpine may also stimulate glands all over the body. A new drug is being used for the treatment of dry eye which is cyclosporine or Optimmune®. This drug has provided relief of symptoms in some patients while other patients have a marked increase in tear production. Unfortunately, a few patients do not respond to cyclosporine and other types of treatment are needed. Cyclosporine offers great hope for the future for humans and for our pets with dry eye.

WHAT IS THE EVENTUAL OUTCOME OF A PATIENT WITH KCS?

Most patients with dry eye will do well if medications are administered on a timely basis. In cases where medicines cannot be given regularly or do not work, surgical techniques must be considered. A parotid duct transposition or PDT (surgical movement of a duct from a saliva producing gland to the eye) is available. The PDT is needed in patients who have had no response to medication or who responded well initially and then had a relapse. In general, with consistent treatment, no patient need lose eyesight due to the dry eye condition.

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Lacrimal Gland Stimulation Protocol

by Dr. Dennis Hacker

Pilocarpine Ophthalmic Solution to be used by mouth

Pilocarpine has side-effects, as do many drugs. One of the effects of pilocarpine given by mouth may be tearing (which is what we are looking for). With higher doses, salivating (slobbering or drooling) is the next most common effect. At still higher doses, vomiting and loose stools may occur. These signs drooling, vomiting and loose stools, are what we are trying to avoid. Unfortunately, we don't know at what level the drug will produce more tears and not cause problems for the rest of the body. Thus, we be adjusting dosage to achieve the desired effect of tearing without the unwanted effects. Pilocarpine should be applied to a small amount of food or in empty gelatin capsules and given by mouth. I find it easiest is to put pilocarpine on a small scrap of bread and give as a treat. Do not just apply drops into the mouth. It is too difficult to get an exact dose and overdoses can occur this way. Within 30 minutes of a dose, tearing should occur and the eyes will look moist if an adequate dose of pilocarpine is given. If given too much pilocarpine, a patient will usually start drooling or may have to get outside to urinate or have a loose bowel movement.

AT ANY TIME, IF THE EYES LOOK MOIST TO YOU WITHIN 30 MINUTES AFTER GIVING THE PILOCARPINE, DO NOT INCREASE THE LEVEL OF PILOCARPINE BEYOND THAT LEVEL WITHOUT CONTACTING THE DOCTOR!

• Start with 1 drop of pilocarpine by mouth 3 times daily for 3 days. Watch for tearing (what we are looking for) or drooling, uncontrolled urinating or loose stools (what we don't want). If you do not notice a change during the first 3 days, on the 4th day, increase the dosage to 2 drops 3 times a day.
• Again, watch for the signs of tearing, drooling, loose stools, or uncontrolled urination. If no change is seen within the next 3 days, on the 7th day after beginning, again increase the dosage by 1 drop (to 3 drops).
• Every 4th day continue to increase the dosage of pilocarpine by 1 drop 3 times a day until your pet either begins to tear within 30 minutes of giving the pilocarpine or drooling or urgent loose stools or urination occur.

IF TEARING OCCURS AT ANY LEVEL, DO NOT INCREASE THE AMOUNT OF PILOCARPINE BEYOND THAT LEVEL WITHOUT CONTACTING THE DOCTOR.

• If drooling, loose stools or vomiting is seen, STOP the pilocarpine for 24 hours and call your veterinary ophthalmologist. Begin at the last level with no side effects. For example, if you get to 6 drops 3 times a day and your pet starts drooling 15 minutes after the pilocarpine is given, STOP the pilocarpine for 24 hours and the next day begin again at 5 drops 3 times daily.

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Lens Luxation or The Loose Lens Condition

by Dr. Dennis Hacker

Within the eye, the chief focusing device is the crystalline lens which is most often referred to as just the lens. The lens is located behind the iris (colored portion of the inside of the eye) within a recess of the ciliary body. When the eye is observed normally, the lens is visible deep within the eye and can be seen through the pupil. Behind the lens is a gelatinous material known as the vitreous body. The lens is normally held within the eye by small fibers called zonules. The zonules are attached to the lens and to the ciliary body to keep the lens in position. Additionally, fluid (aqueous humor) fills the front of the eye (anterior chamber) and is constantly being made and lost from the eye. Aqueous humor maintains the normal pressure of the eye known as intraocular pressure (IOP). The aqueous humor is made by the ciliary body filtering blood. The aqueous humor then normally flows through the pupil and exits the eye to re-enter the blood through small clefts between the cornea (clear portion in front of the eye) and the iris.

What is a luxated lens?

If the zonules break, for any reason, the lens can either become partially loose (subluxated) or completely loose (luxated). When the lens is luxated to the rear (into the vitreous body), it is known as being posteriorly luxated. If the lens is completely loose and falls forward (into the anterior chamber) it is known as being anteriorly luxated.

What causes lenses to loosen?

Several causes of zonular rupture and lens luxation are known: First, in many terrier breeds, lens luxation occurs due to a hereditary rupture of the lens zonules. The condition is most common in the Jack Russell terrier and the Sealyham and Bedlington terriers.

In this terrier, the lens in both eyes has luxated anteriorly. The white arrows demarcate the lens. The black arrows show the area where the lens is absent.

Secondly, any individual patient can develop zonule rupture if there has been serious trauma or inflammation within the eye (uveitis). In cats, subluxated lenses are due to unknown causes and lens luxation occurs most commonly due to uveitis. When uveitis is present, several blood tests are necessary to determine the exact cause of the uveitis in the dog or cat. Thirdly, lens luxations and subluxations may be congenital (present at birth) due to genetic defects. These are seen in very young patients.

Right eye of a young cat with a small lens from birth.

The left eye of the same patient as above.

In both of the above illustrations, the white arrow indicates the lens. The black arrow indicates stretched ciliary body processes. Finally, in any patient, when glaucoma (elevated IOP) has been present for some time, the eye will enlarge and the lens will become loose. For this reason, it is important to discover which came first, the loose lens or the glaucoma.

What are the consequences of a luxated lens?

Because of the flow of aqueous humor through the pupil and out of the eye (as noted above) an anteriorly luxated lens is extremely serious and can cause blinding and painful consequences. An anterior luxated lens will often cause secondary glaucoma or pupillary block glaucoma. This occurs due to the lens (or the vitreous body that also moves forward with the lens) physically obstructing the flow of aqueous humor. Within 72 hours, glaucoma causes irreversible damage to the optic nerve and retina. A posteriorly luxated lens can also cause glaucoma due to a mechanism which is poorly understood.

In this illustration, the lens (white arrow) has fallen backwards into the vitreous cavity. The black arrow indicates the area without the lens.

Liquified vitreous material can obstruct the flow of aqueous humor or the lens itself, which is loose within the eye, can move forward and cause glaucoma as stated above. Additional damage to the eye occurs when the lens is luxated anteriorly. The lens will rub on the cornea and damage or kill the cells which line the cornea (endothelium). The endothelium is important because its main function is to pump into the anterior chamber any aqueous humor which leaks into the corneal tissue. If the endothelium is damaged or are missing, then fluid will collect within the corneal tissue (edema) which can in turn result in recurring painful corneal ulcers and vision loss due to the cornea becoming opaque. Occasionally in cats, the lens will move forward without becoming completely loose. This appears to be due to aqueous humor which normally moves through the pupil into the front of the eye instead goes into the back of the eye into the vitreous body. This results in an elevation of pressure (glaucoma) due to the iris-corneal space being compressed. Lastly, when the lens becomes loose, it will become a cataract.

In this dog, the lens has luxated anteriorly some time ago. A cataract has formed. If the lens has been loose for an extended period of time, the capsule around the lens material may rupture and/or weaken. If this occurs, serious inflammation (uveitis) develops.

What is the treatment for a luxated lens?

The treatment for a luxated lens depends on whether the patient is visual in the affected eye or if there is the possibility of vision. In many patients with a long-standing luxated lens, the lens becomes cataractous (cataract) which obstructs the view of the retina and optic nerve. If a light is shined into the eye with a luxated lens and the pupil of the other eye responds, there is a chance of vision. Because this is not a definitive way to assess vision, an electroretinogram (ERG) will be used in our practice to evaluate the retina. Lens removal surgery is then recommended in a patient with a luxated lens to help the cornea remain healthy and maintain vision. Possible complications of this surgery include the following: Slight bleeding within the eye which usually clears in 1-to-2 weeks. Serious bleeding within the eye which will prevent vision from returning. The lens capsule coming off the lens during surgery which will necessitate a procedure called an anterior vitrectomy needing to be performed. Retinal detachments can occur following this surgery (because this can occur, we perform a laser retinopexy to "spotweld" the retina to HELP prevent this from occuring.) Infections are possible. Chronic uveitis is possible which could require lifetime treatment.

Following lens removal, anterior vitrectomy and laser retinopexy, this is the right eye of the cat above.

Again, the left eye of the cat above following surgery.

If the pupil in the opposite eye does not respond or if the view of the retina and optic nerve reveals severe damage due to glaucoma, then the chance of vision is very minimal. In these patients, lens removal will not restore vision, will probably not restore normal IOP since irreversible damage will have occurred, and may result in intraocular bleeding if iris-to-lens adhesions have developed. If the eye is blind and glaucoma is present, then either a silicone implant inside the eye (an intraocular prosthesis) or an enucleation (removal of the eye) would be best for the patient to relieve discomfort and prevent further complications. One technique employed to result in a cosmetic, pain-free eye for your pet is the placing of an intraocular prosthesis. The technique involves removal of the contents from the inside of the eye--leaving the outer shell of the eye--and implanting a silicone implant within the wall of the eye. The shape of the eye is maintained and the eye moves normally. If you think of making a 'forever' grape by scooping out the insides and placing a marble within the grape skin and finally sewing the skin of the grape closed, you have some idea of how the surgery works.

Following the initial postoperative treatment, minimal care is needed and the eye is maintained in a relatively normal cosmetic appearance while being pain-free. Complications of this technique are that corneal ulceration occasionally occurs in about 3% of patients following surgery (due to drying) and scarring of the cornea (resulting in a gray appearance.) Alternatively, the blind, painful eye may be removed (enucleated). At our hospital, after the eye is removed, an orbital silicone sphere is placed within the orbit, the skin is stitched shut and the hair will re-grow over the surgery site. The use of the sphere gives your pet the appearace of having the eye shut. The possible complication to this technique is possible infection. All surgeries require that your pet be anesthetized.

What about a subluxated lens?

Treatment for lenses which are subluxated depends on whether the IOP is normal or elevated. If the IOP is normal, then ophthalmic drops are used to insure that the pressure remains normal. In this situation, frequent re-examinations are performed over time to assess whether the lens is becoming more loose or is staying in its place. If the IOP is or becomes elevated despite medication, then laser surgery is recommended to help reduce the production of aqueous humor and thus stabilizing the IOP in the normal range.

What about the other eye?

During the initial examination, the opposite eye will be examined to ascertain if the zonules are apparently intact. If the lens appears to be loose due to a hereditary cause, then the lens in the second eye should be removed to prevent the consequences described above. If the lens appears to be normal, then regular re-examinations will be scheduled to assess the beginning of loosening of the lens in the second eye. If the lens in the first eye is loose due to inflammation, then we will attempt to find the cause and treat that cause. In this way, the lens of the opposite eye should stay in its normal position.

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Non-Ulcerative Corneal Disease

by Dr. Dennis Hacker

What is the cornea anyway?

The cornea is the clear portion of the eye located right out front. It is like a sandwich in that on the outside is epithelium just like covers our skin but without hair and normally without pigment. In the dog the epithelial layer is 8-12 cell layers thick. In the cat, the epithelium is 5-to-7 cell layers thick. The epithelium is water-tight so that neither tears outside the cornea nor fluid from within the eye can get past the epithelium. Lining the cornea is one cell layer of endothelium. The endothelium is similar to the cells that line blood vessels. The endothelial cells are leaky. They allow fluid (aqueous humor) from inside the front of the eye (anterior chamber) to leak into the stroma and then the endothelial cells pump the fluid back into the front of the eye via a cellular pump. Between the epithelium and the endothelium is the thickest layer of the cornea, the stroma.

Corneal Dystrophy

What is "Corneal Dystrophy"

Corneal dystrophy is a degenerative change of the cornea in which cholesterol is deposited between the epithelium and the stroma of the cornea. Although the deposits are usually right in the center of the cornea, deposits can occur elsewhere depending on the cause of the degeneration.

This dog has a localized cholesterol infiltrate of the cornea. The white arrow shows the cholesterol.

What do you mean by cholesterol?

Cholesterol is a type of fat or lipid produced by the body. This material is present throughout the body and is responsible for "hardening of the arteries" or atherosclerosis in humans. When present in the cornea, it appears as a "ground glass" appearance and is usually symmetrical. Many breeds develop corneal dystrophy. These breeds include: Afghan, Airedale terrier, Australian shepherd, Basenji, Bearded collie, Bichon frise, Boston terrier, Boxer, Briard, Cavalier King Charles spaniel, Cocker spaniel, Curly coated retriever, Dachshund, Dalmatian, German shepherd, Golden retriever, Irish wolfhound, Labrador retriever, Miniature pinscher, Nova Scotia duck tolling retriever, Samoyed, Shetland sheepdog, Siberian husky and Vizsla. Other breeds and individuals within breeds can develop corneal dystrophy. Dogs with thyroid problems (hypothyroidism) are more likely to have corneal dystrophy, as well as dogs on high fat diets are more predisposed. In addition "dry eye" or KCS could result in dystrophic change in the cornea.

Will corneal dystrophy blind my pet?

It is unlikely for corneal dystrophy to result in complete vision loss. It is possible that a small blind spot can develop resulting in slight vision disturbances.

Is corneal dystrophy painful?

Corneal dystrophy is non-painful in most breeds. In the Shetland sheepdog, changes do occur in the cornea and these pets can become quite painful. Rather than having a single lesion or area of cholesterol infiltrate, shetland sheepdog's develop multiple "coin lesions". In other breeds, if the cholesterol becomes dense enough, it can causes irritation of the cornea. In these patients, blood vessels enter the cornea and pain eventually results. In addition, the patient can develop rather marked vision loss due to the density of the lipids.

What can be done for corneal dystrophy?

For most patients with corneal dystrophy, nothing need be done except determine if an underlying cause is present such as hypothyroidism or high cholesterol in the blood. If the patient is painful, medication containing steroids will be tried initially to try to suppress the inflammation. If this fails, then surgery needs to be performed. The surgery entails surgically removing layers of the cornea until the cholesterol has been completely removed and subsequent use of steroids to prevent return of the lipid. Calcific corneal degeneration

How is calcific corneal degeneration different than corneal dystrophy?

Corneal degeneration refers to any degenerative change in the cornea which is usually post inflammatory in nature. Pigmentation, blood vessels in the cornea and calcium are different components of corneal degeneration. Of these, calcium is the most troublesome.

Calcium has been deposited in the cornea of this dog. The white arrow indicates the calcium with a corneal ulcer within.

What does the calcium do?

Calcium is the mineral which makes bones strong. Calcium is in solution in all tissues of the body. It is present in the fluid within the eye (aqueous) and is constantly moving through the corneal tissue from the inside of the cornea (endothelium) to the surface of the cornea (epithelium). Under certain circumstances, the calcium "precipitates out" of solution either just beneath the epithelium or within the stroma. In these circumstances, the epithelium and stroma of the cornea can become whitish. Sometimes the calcium deposits will coalesce and break through the surface and little chips of the deposit can slough off. Alternatively, the calcium may become quite dense immediately beneath the epithelium. If the calcium becomes thick enough, the surface epithelium can no longer remain attached and will "peel off." The sloughing of the calcium or the peeling off of the epithelium will result in a corneal ulcer which is quite painful.

How is calcific corneal degeneration treated?

If an ulcer is present, the ulcer needs to be treated with topically applied antibiotics to prevent infection while the ulcer heals. Additionally, atropine will be administered topically to dilate the pupil and relax the muscles within the eye which go into spasm when an ulcer is present. Oral Rimadyl® may be given for pain relief to dogs with corneal ulcers. Finally, to help dissolve the calcium, a "chelating agent", ethylenediaminetetraacetic acid (EDTA) will be applied topically several times a day. If the EDTA does not completely remove the calcium, debridement with a diamond burr or a surgical procedure call a superficial keratectomy may be required.

Corneal Endothelial Dystrophy (Endotheliopathy)

What is endotheliopathy?

Endotheliopathy literally means: pathology or disease of the endothelial cells. As stated above, the corneal endothelium is a layer of cells which line the inside surface of the cornea. These cells are similar to those which line blood vessels. Unlike epithelial cells that replicate throughout the life of the patient, the endothelial cells have limited regenerative capabilities depending on the species. In most dogs and rabbits, the endothelial cells will replicate replacing damaged or dead cells. In cats, occasional dogs and humans, the endothelial cells do not reproduce. Also, the epithelial cells are "tight" and do not allow fluid to leak between cells whereas the endothelium is "leaky". The endothelial cells allow the leakage of fluid (aqueous humor) from the front of the eye (anterior chamber) into the corneal stroma and then the endothelial cells normally pump the fluid out of the cornea back into the anterior chamber. The cornea is normally clear despite being bathed in tears on the outer surface and bathed with aqueous humor on the inner surface. This clarity is maintained by the function of this endothelial cell layer. If the endothelial cell numbers are reduced or if they cannot perform their function, the aqueous humor will build up and the cornea will become hazy. The build up of fluid is called corneal edema. In severely affected dogs, the cornea contains enough fluid that bullae or vesicles (medical words for "blisters") form. These are similar to tiny blisters on the skin. The condition in people is called Fuch's endothelial dystrophy, named for Dr. Fuch who was the first to describe the condition in medical literature. Fuch's dystrophy is more common in elderly women than men. Edema can also occur from inflammation within the eye (uveitis) or from high pressure within the eye (glaucoma) which interfere with the endothelium performing its normal function. The fluid build up progresses at varying rates in different pets. The edema will eventually lead to blindness. This is a slowly progressive disease, for which there is no cure.

Diffuse haziness to the left cornea of this patient is the symptom of endotheliopathy.

The right eye of the same patient is normal.

Which animals get endotheliopathy?

Corneal endothelial dystrophy is an uncommon condition, but is seen most frequently in the Standard poodle, Chow chow, Dachshund, Boston Terrier and Chihuahua. Age of onset is generally 7 to 9 years of age. Additionally, a similar condition has been reported in the Manx cat. We have seen this condition in individual dogs of various breeds. These are usually older patients. The cause of the loss of endothelial cells is not known although the breed distribution suggests an inherited predisposition, along with normal loss of the endothelial cells due to age.

How is endotheliopathy treated?

As mentioned above, in severely affected individuals, blisters or bullae form within the cornea. These will break resulting in a corneal ulcer which is painful. If a corneal ulcer is present, it will be treated with topically applied antibiotics and atropine to prevent infection and relieve pain. Additionally, application of topical hyperosmotic eye ointment containing 5% NaCl, may help reduce bullae formation, but the corneal edema does not clear. Corneal transplantation is the treatment of choice for Fuch's endothelial dystrophy in humans. Corneal transplants have been tried in dogs, but the success rate is less than desirable until recently. The reason that success rates have been low includes the fact that the dog's cornea vascularizes more readily that the human cornea which promotes rejection (vascularization and scarring) of the graft. Newer medications such as cyclosporine hold promise for increases in the success of corneal transplants in our pets.

Finally, for those pets who do not have a corneal transplant, the fluid build-up will worsen and they will continually develop corneal ulcers. As an alternative to the corneal transplant, a surgical treatment known as thermokeratoplasty is used to make small lesions on the surface of the cornea which in turn causes blood vessels to enter the stroma. These blood vessels help draw out the aqueous fluid, which causes the edema, before bullae or vesicles develop. Once this procedure is performed, a corneal transplant CANNOT BE PERFORMED because the presence of the blood vessels will guarantee failure of a graft.

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Pannus (Chronic Superficial Keratitis)

by Dr. Dennis Hacker

(Chronic superficial keratitis) Pannus, or chronic superficial keratitis, is a slow progressive degenerative disease of the dog's cornea. Pannus leads to brown or pink tissue ingrowth, blood vessel ingrowth and scarring. Pannus leads to a slow loss of vision. This condition is seen predominantly in German Shepherd dogs, but occasionally is seen in other breeds as well.

Cause

Although many infectious agents have been suggested none have been shown to cause the condition. The actual cause of pannus is not known.

Several factors are thought to be involved:

• The fact that it is commonly seen in German Shepherd dogs suggests a hereditary predisposition.
• Ultraviolet radiation may play a role as an inciting agent and cause worsening of the condition. Dogs living at high altitudes often are more severely affected.
• Immune factors are believed to contribute to the severity of this disease. This may be allergic-type reactions against materials from outside the body or against the corneal tissue itself.

Signs

Initially, redness and brown pigment may be seen in the conjunctiva (white tissue of the eye). White infiltrates made up of inflammatory cells then invade the clear cornea. Next blood vessels invade the cornea. Finally pink connective tissue grows into the cornea and later becomes brown. In a small number of cases, two other symptoms may occur either alone or together. A thickening, redness, depigmentation and lumpiness of the third eyelid may occur. This is called a plasmoma. The other condition which may occur is chronic, erosive ulceration of the lower eyelid near the inner and outer corners of the eye. Pannus is uncomfortable to the dog. When treated adequately, your pet can be free of this irritation even though the corneas may not clear up completely.

Diagnosis

The clinical findings usually are typical enough for a diagnosis to be made for routine pannus. Ocassionally, a biopsy is needed of the eyelid and third eyelid tissue to rule-out cancer as the cause of the ulceration.

Treatment

Despite intensive research efforts, no permanent cure exists for pannus. However, in the vast majority of cases, the disease progress can be halted and the problem kept stable. In other cases, pannus may be reversed and the corneas will clear. This is most probable if therapy is instituted early during the disease. The inflammatory cell infiltrate and blood vessel invasion are generally reversible with therapy. The connective tissue infiltration and pigment deposits are often not reversible once they have occurred.

There are four types of therapy

• Corticosteroid (cortisone) therapy. This is the main line of defense against progression of the disease and in most cases is effective. If the pannus is severe, cortisone may be administered by injections under the white of the eye. In all cases drops containing cortisone must be applied to the eye many times a day. Treatment must be kept up for the rest of the pet¹s life. Even short periods of interrupted treatment, i.e., 2-to-4 weeks, may cause severe relapse with worsening of the patient's vision. The main side-effect of prolonged corticosteroid therapy is the adverse effect on corneal wound healing. Microscopic wounds of the outer layer of the cornea often occur. In a normal eye the cornea heals rapidly. If corticosteroid medications are being applied, minor wounds worsen leading to serious corneal ulceration. The main sign seen in patients with ulceration is pain. Therefore, should any patient on cortisone therapy show signs of pain, such as holding the eye shut or pawing at the eye, it is important that the medication be stopped and the doctor consultedimmediately.
• Cyclosporine is a new medication in the war on pannus. It does work on pannus and doesn't have the side effects of corticosteroids. Unfortunately, cyclosporine doesn't work as quickly and it is usually necessary to continue it twice daily for the rest of the patient¹s life. Often, we will initially prescribe corticosteroids to be used in addition to the cyclosporine. When used together, greater improvements are seen without the side effects associated with high levels of corticosteroids.
• Surgery may be used when medication does not completely clear the pannus from the cornea. A 'peeling' of the cornea may be required to restore vision in eyes that are severely scarred and pigmented. Unfortunately, treatment is required following surgery to prevent the pannus from recurring as the cornea heals. This method is only used if medication doesn¹t work.
• Beta-irradiation may be used when medication and surgery prove insufficient. This will not be recommended unless all else fails. Pannus can be a frustrating condition that requires life-long treatment. Yet with the correct diagnosis and early treatment, vision can be maintained

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Persistent Pupillary Membranes

by Dr. Dennis Hacker

During development, the iris (colored portion inside the eye) first forms as a solid sheet of tissue. Late in gestation a breaking down of tissue takes place to form the pupil. If some of these fine strands of tissue remain they are described as persistent pupillary membranes (PPM). It is not unusual to see such strands in 6-to-8 week old puppies or kitties. However, if they persist beyond this this age they are considered a defect. They can form attachments between the cornea and/or the lens resulting in opacities and cataracts and can cause vision defects. In the Basenji and Mastiff breeds, this anomaly has reached such proportions as to be considered a major inherited ocular disease. In 6-to-8 week old Basenji and Mastiff puppies if the strands are extremely large or if they persist beyond the 12th week a note should be made on the examination form. This problem is becoming more recognized within the Collie breed. Other breeds may have individual animals with PPM as a problem.

The arrows point to persistent pupillary membranes in this dog. The adjacent white specks are scars on the inside of the cornea due to the membranes touching the cornea.

This cat has persistent pupillary membranes pointed out by the arrows. The persistent pupillary membranes lead from the iris to the lens where they are causing a focal cataract.

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Progressive Retinal Degeneration and Atrophy

by Dr. Dennis Hacker

Progressive retinal degeneration (PRD) [also known as progressive retinal atrophy (PRA)] refers to several different retinal diseases that cause blindness. There are two distinct patterns to this disease. Some breeds have blindness by abnormal development (dysplasia) of the retina. Other breeds have a slow progressive death of retinal tissue (degeneration). These two types of disease affect many breeds. In general these diseases are inherited. The pattern of inheritance may be different in each breed. In all patients with PRD the outcome is the same--blindness.

The age and breed of the patient and what the Veterinary Ophthalmologist finds during the examination are the basis for the classification of exactly what type of condition the patient has. Different breeds of dogs have variations in the age at which the problem starts and speed with which the blindness develops. The condition of PRD has been seen in almost every registered breed and in mixed breed dogs as well. This condition occurs in humans and is known as retinitis pigmentosa. As the name PRD implies, a slow degeneration or death of retinal tissue occurs. It is a slowly progressive disease and the earliest signs may be overlooked. As stated above, PRD or the gene for PRD is known to be passed from parents to offspring even though the parents may have normal eyes and vision. Therefore, identification of breeding animals with or related to patients with PRD is essential to prevent spread of this condition. At this time, researchers are working to find a blood test to identify "carrier" animals.

To better understand PRD, a basic understanding of the function of the retina is needed. The retina is a highly complicated tissue located in the back of the eye. Light strikes the retina and starts a series of chemical reactions that causes an electrical event (nerve impulse). The impulse passes through the layers of the retina to the optic nerve and from there to the brain where vision takes place. In the retina, cells called rods are involved with black and white or night vision and cells called cones are involved with color or day vision. Progressive retinal degeneration may effect either the rods alone, the cones alone or both the rods and cones together. Because PRD is not a painful condition your pet will not have reddened eyes or have increased blinking or squinting. For this reason most clients will not notice the earliest stages of the condition. Some clients will eventually notice an abnormal shine coming from their pet¹s eyes. This abnormal shine is because the pupils are dilated and don¹t respond as quickly to light as pupils of normal dogs. Early signs of PRD include night vision difficulties. Clients often remember their pets seemed disoriented when going out to the yard at night and they had to leave a light on for them.

Night blindness may be manifested by a pet that is afraid to go into a dark room. Occasionally these pets will become lost in their own home after the lights have been turned off. The Veterinary Ophthalmologist examines the retina with an instrument called an indirect ophthalmoscope. Specific changes in the retinal blood vessel pattern, the optic nerve head, and the reflective substance within the dog¹s eye (tapetum) are classic for PRD. However in some breeds PRD has little or no early changes. The eyes of these dogs may appear normal on the examination until they are in the later stages of the disease. In different breeds, PRD will progress at different rates. This variation causes difficulty in determining just how long any particular dog will be able to see. There are no cures for PRD although a number of vitamin therapies have been suggested by various people. At this time, none of the vitamin treatments have been effective and some of these 'cures' may actually hurt your pet.

Cataracts may occur in some patients with PRD and generally occur later in the disease. Formation of cataracts may interfere with the Ophthalmologist's examination of the retina and make other tests such as an electroretinogram (ERG) essential for accurate diagnosis. In patients with cataracts the diagnosis is made and confirmed by the ERG. This test involves sophisticated instrumentation used to measure the response of the retina when a light is shined upon it. Your pet would be anesthetized for this test. The pet is then placed into a darkened area, a special contact lens with a gold ribbon is placed on the cornea and two tiny needles are placed under the skin. A dim light flash stimulates the retina and this procedure is repeated for 20 minutes. Finally, a bright red, blue and white flash are used for final analysis. A healthy retina will produce a characteristic wave that builds from the time the lights are turned out. The ERG is sensitive enough to diagnose dogs with PRD before they begin to demonstrate signs of the disease. Here is a partial list of breeds affected with different types of PRD:

BREED	TYPE OF RETINAL DISEASE	AGE OF ONSET
Collie	rod-cone dysplasia	under a year
Irish Setter	rod-cone dysplasia	under a year
Cairn Terrier	rod-cone dysplasia	under a year
Miniature Longhair Dachshund	rod-cone dysplasia	under a year
Norwegian Elkhound	rod dysplasia, cone degeneration	2 to 3 years
Samoyed	rod-cone degeneration	3 years
Cocker Spaniel	rod-cone degeneration	2 to 7 years
Miniature Poodle	rod-cone degeneration	6 mo. to 5 years
Miniature Schnauzer	rod-cone degeneration	3 to 6 years
Akita	rod-cone degeneration	3 to 6 years

In summary, PRD refers to a group of inherited retinal diseases which result in the blindness of dogs. Because of the nature of the disease and sometimes the late onset, repeated examinations may be required to detect individuals with the condition. Patients affected should not be used for breeding. Pedigree studies are used to help eliminate carriers of this condition such as the pet¹s brothers, sisters, mother, father and any offspring. How to adjust to having a pet that is blind is important and is discussed in the information on "Dealing with a blind pet.".

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Red Eye

by Dr. Dennis Hacker

Unlike humans, when dogs and cats have a "red eye", they do not have a bacterial conjunctivitis or "pink eye". They are not susceptible to the bacteria which causes pink eye in children. When a veterinary patient is presented with what is described as conjunctivitis, several conditions must be considered.

What is Conjunctivitis?

Conjunctivitis simply means that the conjunctiva, the moveable white tissue seen when we look at each other¹s eyes, is inflamed. It does not describe the cause. Conjunctivitis is described in people as an itchiness and is described as not painful.

What are the causes of a "red eye"?

In the dog, causes of a red eye include keratoconjunctivitis sicca, glaucoma, uveitis, episcleritis, foreign bodies, eyelash disease and allergy. In the cat, causes of a red eye include keratoconjunctivitis sicca, uveitis, herpesvirus infection , eosinophilic conjunctivitis, chlamydia infection, mycoplasma infection, foreign bodies and allergy.

What is Epislceritis?

Episcleritis is an inflammation of the outermost layer of the external wall of the eye (sclera). Episcleritis is divided into three classifications depending on the clinical appearance: erosive, proliferative or diffuse. Erosive episcleritis is the most severe in that the wall of the eye is "eaten" by inflammation and the wall of the eye can rupture. This type of epislceritis requires surgery to strengthen the wall of the eye. Proliferative episcleritis appears as a thickening of the outer wall of the eye or a thickening of the inner eyelid.

The arrow indicates a proliferative lesion of episcleritis. These lesions can lead to corneal ulcers adjacent to the lesions due to an area of drying occurring when the tear film cannot spread evenly over the eye. Alternatively, the lesion may itself spread into the cornea resulting in episclerokeratitis.

In this dog, the pink, fleshy lesion has spread into the cornea resulting in episclerokeratitis.

Diffuse epislceritis appears as an area of redness which may worsen in degree of redness and enlargement of area. Episcleritis is most commonly seen in the Collie, Rottweiler and American Cocker Spaniel although any breed of dog can develop the condition. Ofttimes, an area of cholesterol may be present in the outermost layers of the cornea following the inflammation of episcleritis. Diagnosis of epislceritis is by biopsy (if proliferative) or cytologic examination. Treatment of epislceritis is either steroids, cyclosporine or a combination of both. Additionally, oral antibiotics and vitamin B6 may be given. If these do not work, then an oral immunesuppressive medication (Imuran®) is used. What is an Allergy? Allergic conjunctivitis may be due to pollen, house dust mites, molds, mildew and food allergy as well as odors from new carpets and recently finished floors. There is no way to diagnose an allergy directly. For this reason, allergic conjunctivitis is a diagnosis of exclusion, that is we exclude all other causes and what is left is allergy. The treatment for allergic conjunctivitis is either steroids or nonsteroid antiinflammatory drugs (NSAIDs). If a cause can be determined, the elimination of the cause will often result in the resolution of the allergy.

What is Eosinophilic Conjunctivitis?

Cats can develop a specific type of conjunctivitis known as eosinophilic conjunctivitis. The diagnosis is made by performing a conjunctival scraping and examining the cells with a microscope. The predominant type of cells is a white blood cell known as the eosinophil. It is called this because of the way it retains stains. Although the cause for eosinophilic conjunctivitis is unknown, several causes of eosinophilic conjunctivitis have been proposed. These include herpesvirus, allergy and other virus infections. Herpesvirus must be ruled-out as a cause because treatment for eosinophilic conjunctivitis is topically applied steroids or oral steroids or megesterol acetate.

Are there infectious causes of Conjunctivitis in the cat besides Herpesvirus?

Cats may develop a respiratory condition (called URI) from herpes, mycoplasma or chlamydia. The most common cause of conjunctivitis in the cat is Herpesvirus. This virus is a common cause of upper respiratory disease in cats. It is passed in droplets when the cat sneezes or coughs. Other causes of respiratory disease and conjunctivitis are Chlamydia and Mycoplasma. Like viruses, they live within the cells of the respiratory tract and the conjunctiva. These conditions are most commonly found in the kitten, rather than older cats but can be found in any cat of any age. Whilst these pathogens are not extremely common, they do cause a lot of problems, especially in catteries. These organisms are smaller than bacteria and larger than viruses. Herpes is discussed in another handout. Chlamydia is an infection with a rickettsial agent. Rickettsia agents are not really bacteria, although they can be killed with specific antibiotics and not really viruses although they act like viruses because they need to live inside cells. Chlamydia is in the same family as the agents which cause Rocky Mountain Spotted Fever. Mycoplasma is similar in that it lives on the outside of cells and needs cellular material to live and can be killed by specific antibiotics. Both of these organisms cause URI and conjunctivitis, which can be quite dramatic. Neither of these can cause corneal ulcers. Both can be a simultaneous infection with herpes. We can detect chlamydia and mycoplasma by scraping the white of the eye and examining the stained slide using a microscope and looking for characteristic findings (inclusions). The inclusions are not commonly found in scrapings from patients with a long-standing or chronic condition. Finding the inclusions is usually diagnostic although other laboratory tests can confirm the findings, especially in chronic cases. Treatment is with either antibiotics applied to the eyes or oral Zithromax®. If medication is given and the patient doesn¹t respond as expected, tests for herpes may be warranted.

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Retinal Dysplasia and Retinal Folds

by Dr. Julie Gionfriddo, D.V.M., Dip. A.C.V.O. and edited by Dr. Hacker

Anatomy and Physiology

The retina is the structure inside 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 in the brain this is how we see. The development of the retina when we are in our mothers is quite complex. The eye develops from a small section of the front of what becomes the brain of the adult. Malformations of the retina before birth can occur and may be due to either hereditary, toxicity or virus infection.

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 developmental layers of the retina do not unite properly. When this occurs, it is just like taking two different lengths of material and sewing them together. Folds or larger problems may develop. Dysplasia may manifest as folds in the 'inner retinal layer'. These are called "retinal folds". In "geographic" retinal dysplasia there are larger areas of abnormal retinal development. In the most severe form of dysplasia, the 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 re-examination is recommended 6 months later 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.

Retinal folds in the tapetal fundus of a puppy (arrows mark folds).

Retinal folds along the blood vessels of the retina (arrows mark some of the folds).

Affected Breeds Retinal dysplasia is reported in 25 of the more than 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. In many breeds ophthalmologists and researchers have not determined exactly how retinal dysplasia is passed. In the Labrador retriever and Samoyed breeds, a combination of retinal dysplasia and skeletal defects (dwarfism) 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 (animals with two identical genes, one from the mother and one from the father) have skeletal changes and mild-to-severe retinal dysplasia while heterozygous animals (different genes one from the mother and one from the father, only one of which is abnormal) usually have just mild retinal dysplasia. Retinal folds rarely cause vision problems for the individual dog. They represent small blind spots which are 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 whether dogs with retinal folds will "pass" a CERF examination. Retinal folds may be seen in certain breeds and still pass a CERF examination and receive a CERF number. This is due to the fact that the condition is thought to either not 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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Systemic Hypertention

by Dr. Dennis Hacker

Frequently, a concerned client will present a cat or, less frequently, a dog to their regular veterinarian with the complaint that one or both eyes was or currently is red inside. Most of the time the veterinarian will examine the eye and diagnose inflammation (uveitis) or injury as the cause of the redness. In some cases, this diagnosis is correct. Unfortunately, in some cases this diagnosis is incorrect. A significant condition which isn't often diagnosed until the patient is blind or has a stroke is called "systemic hypertension" or high blood pressure.

What is systemic hypertension?

In humans and pets, two types of high blood pressure are recognized--essential (due to unknown cause) and secondary (due to some underlying disease). In humans, essential hypertension is the most common type. Secondary hypertension is the most common type in veterinary medicine.

The most common causes of hypertension in dogs include kidney disease, adrenal disease, hypothyroidism (underactive), diabetes and pituitary tumor. In cats, kidney disease, hyperthyroidism (overactive) and heart muscle disease are the most common causes. In humans, systemic hypertension is called the 'silent killer' because there are no characteristic feelings or outward symptoms or signs of high blood pressure until a stroke occurs.

If people cannot tell they have high blood pressure, how can our pets be expected to "tell us"? What is normal blood pressure? In humans, our blood pressure is often reported as being normal at 120/80 millimeters of mercury (mm Hg). The first number (120 mm Hg) is the systolic pressure or how much force the heart exerts to push out the blood. The second number (80 mm Hg) is the diastolic pressure or the resting tension of the arteries (blood vessels which carry blood from the heart to the body organs). In veterinary medicine, we cannot always get a diastolic reading because of patient anxiety or noise in the environment. Normal blood pressure in the dog and cat is less than 160-170 mm Hg systolic.

How is a blood pressure reading obtained?

A blood pressure evaluation is performed every time you are seen by your regular physician and we are familiar with the technique. In veterinary medicine, we cannot get the blood pressure exactly as it is done in humans, but it is most frequently done in a similar manner. At research institutions, blood pressure is measured via the 'direct' method. In this technique, a needle is threaded directly into an artery and the blood pressure is measured through a complicated piece of equipment known as a pressure transducer. This technique can be extremely accurate but is difficult to perform and your pet does experience slight discomfort.

The second, and most commonly performed method, is the 'indirect' method. It requires an amplifier and a pressure sensor instead of a stethoscope. A small 'cuff' is applied around the patient's leg and the pressure sensor is placed on an area of skin where the fur is clipped at the 'wrist' or 'ankle'. After this preparation, the technique is then almost exactly the same as with humans. Because of the expense of the equipment, I would estimate that less than 10% of veterinary hospitals have indirect blood pressure equipment.

What are some of the signs of high blood pressure?

The typical patient seen in our referral ophthalmology practice is a dog or cat who is over 10-years old and seems healthy to the client. The cat could have had redness to one or both eyes which came and then resolved once or maybe twice before. Alternatively, the client may have noticed that the cat's pupils were becoming more and more dilated and now the cat appears blind. When taken to the regular veterinarian, blood work, a physical examination and perhaps x-rays were done and medication prescribed which didn't help.

Dogs and cats may have nose bleed, weight loss, increased thirst, increased drinking and weight loss or abnormal "neurologic" signs. During the examination at our hospital, blood may be found in the front of the eye (hyphema) or behind the lens inside the eye (intravitreal hemorrhage) OR one or both retinas are found to be detached (retinal detachment) with no signs of inflammation. Occasionally, the findings will be that of small hemorrhages (bleeding) within or beneath the retina or we will find extremely dilated blood vessels in the retina. These hemorrhages are not visible without a complete eye examination.

We will then perform the 'indirect' blood pressure test and usually find that the patient¹s blood pressure is over 200 mm Hg and sometimes the blood pressure will be greater than 300 mm Hg! Many times, clients aren't even aware of a problem due to hypertension in their dogs.

What are the causes of and treatment for hypertension?

In both dogs and cats, kidney disease is the most common cause of systemic hypertension. Because kidney disease can cause hypertension and hypertension can cause kidney disease, many different parameters and blood tests must be evaluated. The above systemic conditions should be ruled out and medication needs to be staarted. Medication is usually a tablet given by mouth once or twice daily. For cats who are difficult to give tablets to, the medication can be prepared in a fish or chicken flavored base and given as a liquid.

Once medication is begun and once the blood pressure is stabilized in the normal range, the blood tests must be repeated to assess what happens to the kidneys and other body organs when the blood pressure is lowered. As in people, blood pressure medication must be continued for the life of the pet.

Is blood pressure evaluation necessary?

Blood pressure evaluation is very necessary in older dogs and cats. Early detection and treatment can help prevent blinding and fatal complications such as stroke. I would recommend that a blood pressure reading be performed on an annual basis for every pet over 10 years of age or any pet displaying chronic kidney disease or any nose bleed or redness (blood) inside the eye.

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Sudden Acquired Retinal Degeneration (SARDS)

by Dr. Dennis Hacker

Veterinary ophthalmologists have identified a condition of rapid onset of blindness. This condition, known as Sudden AcquiredRetinal Degeneration (SARD), may strike any breed of dog.

In some patients there are increases in appetite and water consumption. Pets who develop SARD are often older than 6 years of age. Examination of tissue specimens from some patients at research institutions has indicated that the retina in these pets is totally destroyed and cannot regenerate. Blindness occurs essentially overnight.

A typical pet would have gone out on a walk with the client one day or evening and been normal. The next day, the patient would begin to bump into everything in the house. Examination by a Veterinary Ophthalmologist reveals that the patient has normal eyes with no evidence of significant cataract development and no evidence of apparent retinal disease.

The pupils will occasionally, but not always, respond to light but the patient is blind! Because there are no ophthalmic findings which indicate SARD, patients with apparently normal eyes and acute vision loss should have blood tests performed to rule-out systemic disease as a cause of blindness. The non-systemic conditions which can mimic SARD are brain tumors and optic nerve inflammation (optic neuritis).

The reason the diagnosis is important is that if systemic disease or optic neuritis is causing the blindness medication may restore vision. If a brain tumor is determined to be present, then radiation therapy may be necessary to save your pet's life. For these reasons, finding the cause of sudden blindness is important!

The first step in diagnosing the cause of blindness is a thorough ophthalmic and physical examination and blood tests. Next, a test of the retina known as an electroretinogram (ERG) should be performed. If the retina is working normally, then further tests are needed to determine the diagnosis.

As with other types of retinal degeneration, SARD has no treatment. Although veterinary ophthalmologists do not completely know the cause of and cannot treat SARD, you should know that this is not a painful condition. Your pet is not in pain. Your pet is just confused as you would be if you suddenly went blind.

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Toxoplasmosis

by Dr. Dennis Hacker

What is this condition?

Toxoplasmosis is caused by a common parasite or one-celled organism (protozoa) called Toxoplasma gondii. Blood tests in the United States suggest that about 30-40% of humans and 15-65% of cats have been exposed to this parasite and have developed a reaction (or antibody).

How is Toxoplasmosis passed from one animal to another?

The life cycle of Toxoplasma gondii consists of what are termed a sexual phase and an asexual phase. Cats are the definitive host and the only species in which the parasite can complete the sexual phase of its life cycle. The sexual phase results in the passage of oocysts (similar to eggs) in the feces. In approximately 3 days from being passed in the stool, the oocysts matures and develops spores (sporulate) within the oocyst capsule before they become infective to other animals (intermediate hosts). Intermediate hosts include most species of mammals (including humans), birds, reptiles and fish. These intermediate hosts become infected by ingesting sporulated oocysts in contaminated food or water. The oocyst capsule ruptures and spores (sporozoites) infect cells lining the wall of the intestinal tract. The sporozoites burst through the intestinal lining and then spread to various parts of the body of the intermediate host where they eventually lodge. The immune system of the intermediate host forms a wall around the parasite (encyst). If a female animal is pregnant, sporozoites can spread to the placenta during this phase of infection and infect the fetus. The asexual phase of the parasite's life cycle occurs when an animal ingests cyst infected meat from other intermediate hosts (fish, chickens, beef and pork). The parasite's life cycle is completed when a cat eats meat infected with cysts and the life-cycle starts all over again.

Does Toxoplasmosis cause problems in Cats?

The cat is the only species in which the parasite can complete both the sexual and the asexual phases of its life cycle. Most cats get infected as intermediate hosts soon after weaning either by being fed raw infected meat or by catching and eating infected rodents. The incidence is higher in feral (wild) and outdoor cats than cats who always stay indoors. During the sexual phase of toxoplasmosis, infected cats shed oocysts in the feces for 1-3 weeks after the initial infection. Once a cat has been infected and shed oocysts once, it rarely will shed them again. The intestinal phase of infection does not cause significant clinical problems in the cat. It is the asexual phase that can cause disease especially in immunodeficient cats including young kittens and cats infected with the Feline Leukemia Virus (FeLV) or the Feline Immunodeficiency Virus (FIV or feline AIDS virus). The signs of toxoplasmosis include weight loss, fever, lethargy, neurologic or respiratory problems and eye problems. The eye problems include inflammation (uveitis), glaucoma (high pressure), retinal detachment and blindness.

What problems does Toxoplasmosis cause in Humans and Dogs?

Humans and dogs can become infected with Toxoplasma gondii by ingesting sporulated oocysts or tissue cysts, or through the placenta (transplacentally). In normal adults, the infection is generally a flu-like condition. Transplacental infection occurs when a pregnant woman is exposed and infected during the first 2 trimesters. Approximately 50% of the fetuses may be infected and severe clinical disease may develop in some of these (about 10%) newborn children. Clinical signs include abortion, stillbirth, hydrocephalus (water on the brain), eye problems and neurologic disease. These problems occur because the infection occurs prior to the development of the immune system. As the immune system develops, the body sends out "messengers" to sample all the parts of the body that it can. All these things are then considered "SELF" and, unless abnormal conditions occur, the individual doesn¹t try to fight off those "self" things. The baby's immune system then considers the parasite as part of the baby and the immune system doesn't try to wall off or kill the toxoplasma organism. Immunocompromised individuals (organ transplant recipients and AIDS patients) are also at risk of serious disease from Toxoplasma gondii for the fact that they can't fight off the parasite. An immunocompromised person may have the tissue cysts from prior infection reactivated. Handling cats is not considered a major risk even in immunodeficient people. People are probably at greater risk of contracting the disease while working in their gardens or preparing dinner than when employed in a kennel situation. Dogs who are on high doses of corticosteroids for any number of problems are at the same level of risk as the immunocompromised human. Dogs can also acquire the infection by eating cat feces found in the yard, parks or the family litter pan. About 30-40% of women of child-bearing age have antibodies to toxoplasmosis indicating previous infection. These women are not at risk of transmitting the infection to their fetuses. That leaves 60-70% of women at risk. It is estimated that there is about 1 infected child born per 1000 births or somewhat over 3000 babies per year in the US. Oocysts can live in the environment for long periods and most human and dog infections probably result from contact with contaminated soil or water. Gardens and sand boxes are frequently used by cats for defecating and may be contaminated. Oocysts can be transported by accidental hosts such as cockroaches and flies which in turn can contaminate surfaces and food. Raw or undercooked contaminated meat is a major source of infection for humans and their pets. Pork products in the US have a high incidence of tissue cysts, but fish, chicken and other types of meat may be infected. Milk can also be contaminated. Most cow's milk is pasteurized, but goat's milk is frequently consumed raw. Vegetables may be contaminated by soil or accidental hosts. Cooking for 20 minutes to an internal temperature of 150 F will kill tissue cysts and freezing to -200 F for several days will reduce the number of cysts. Rubber gloves and regular hand washing will minimize the chance of infection. The sporulated oocysts in the environment and tissue cysts are infective immediately and protective measures are much more important here than when handling and caring for cats.

How can infection in Humans be prevented?

Infection from direct contact with cats shedding oocysts is not very likely. Cats only shed oocysts for a few days to weeks in their lives after primary infection. Cat feces are generally firm and cats do not soil their coats or they groom away any feces quickly. As stated above, it takes several days for the oocyst to sporulate and become infective, thus fresh feces are not contagious. Wearing rubber gloves and washing hands after cleaning litter boxes will prevent infection. Clothes or coveralls worn when cleaning cat pans and cages should be washed after each use. Cat feces and litter dust are not likely to be a source of human infection in the context of a kennel situation if the litter is changed daily and the pans are disinfected by steam or hot water.

How is Toxoplasmosis detected?

Numerous tests for antibody (body's reaction) to toxoplasma can be used to detect infection in humans and other animals (dogs and cats). Many of these measure blood antibodies (Immunoglobulins [Ig] G [IgG] and M [IgM]. The IgG titer may remain high for months to years in cats and is not a good test for recent infection but does tell of past infection. The IgM titer is a better indicator of recent infection. The IgG and IgM titers do not indicate the likelihood that the cat is currently passing oocysts because they indicate infection during the asexual and not the sexual phase. (Remember, oocysts are only passed in the sexual phase and the cat doesn¹t get ill from the sexual phase.) Fecal exams for the detection of oocysts can be done, but the oocysts may be missed and it is a rather laborious procedure.

How is Toxoplasmosis treated in cats and dogs?

When a cat or dog is systemically ill with toxoplasmosis, there are several medications that can be used. Clindamycin (Antirobe®) or trimethaprim/sulfa drugs (Tribrissen® or DiTrim®) are the best choices. These have to be given for 6 weeks. These drugs can cause an upset intestinal tract and may cause vomiting or diarrhea.

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Uveitis

by Dr. Dennis Hacker

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. Inside the eye, the innermost layer is the nerve layer or the retina.The middle layer of the eye (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 the part of the eye which produces the fluid inside the eye (aqueous humor) and the choroid that provides nutrition to the retina inside the eye.

When inflammation develops within the uveal tract, the term is uveitis (-itis means 'inflammation of', so this is inflammation of the uvea). As specific segments of the uveal tract are affected, uveitis 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. These are doctor terms but are helpful for you to know. Due to its rich blood supply, the uveal tract is a natural target for diseases originating in other parts of the body. Because the cornea is normally clear, signs of disease may be seen inside 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), on the surface of the eye (such as corneal ulcer) and trauma.

Diagnosis of uveitis

Uveitis is not a disease just as a sprained ankle or a sore throat aren't diseases. It is a condition or syndrome which indicates inflammation within the eye.

Uveitis may cause vague clinical signs that may include blinking, squinting, watery discharge from the eye, and/or fear of light (photophobia) without any obvious changes to the eye itself. The normally clear cornea may appear dull or hazy 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 (colored portion of the eye) becomes red or changes color. 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 certain diseases are 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. (This is not tears!) 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 or a membrane might develop over the iris and drainage angle and inhibit the outflow of the fluid causing elevated intraocular pressure (IOP). This is known as glaucoma. Alternatively, the iris may adhere to the lens and block fluid flow through and out of the eye resulting in glaucoma .

Once uveitis resolves, glaucoma may persist if drainage structures were permanently damaged by the inflammation or the membrane. Alternatively, if the ciliary body has been severely damaged, fluid production may cease entirely and the eye will begin to shrink up. Recheck of the eyes following the resolution of uveitis is important for these reasons.

Causes of uveitis

Uveitis may be caused by many different diseases. Diseases in the dog include lymphoma, bleeding disorders, 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 and/or other diseases.

In any animal, a corneal ulcer or penetrating injury such as cactus spines, porcupine quills, pellets or b.b.'s or a scratch may result in uveitis. Blunt trauma can damage the eye severely and result in uveitis. Inflammation of the uveal tract can occur when the lens leaks some of its contents inside the eye. The lens may cause uveitis when injured, when a cataract is rapidly forming, when cataract is dissolving or following penetrating injury or certain types of surgery such as cataract 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) or Rimadyl® by mouth and indomethacin, Profenal®, Ocufen®, Voltaren® and corticosteroids (cortisone drugs) minimize the inflammatory process. Corticosteroids may be administered by injection under the conjunctiva (moveable white tissue of the eye), by eye drops or as an oral medication or a combination of these means 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. Rymadyl® is an oral non-steroidal antiinflammatory drug (NSAID) which can be given by mouth to dogs and by injection to dogs and cats. Indomethacin, Voltaren®, Ocufen® or Profenal® drops are topically applied NSAID's 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 often not used because bacterial infections are not commonly found as the cause of inflammation

Certain bacterial agents can cause uveitis in conjunction with the systemic infection. In these cases, such as Ehrlichia, Lyme's disease and Rocky Mt. Spotted Fever, antibiotic medication must be given to prevent worsening and recurrence of the uveitis.

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 lifelong. In other patients, uveitis is so severe that removal of the eye is necessary. Lastly, in occasional patients, uveitis is self-perpetuating (causes more uveitis). These patients are difficult to control.

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Vitreous Degeneration

by Dr. Dennis Hacker

What is vitreous?

The vitreous is a jelly-like material located behind the lens in the eye. It has several responsibilities. First, it helps keep the retina in position. Second, by being a jelly, it reduces torque applied to the retina when an individual shakes their head.

What is vitreous degeneration?

Vitreous degeneration may be one of several conditions: It may refer to liquification of the vitreous which occurs following some types of inflammation. This occurs commonly in horses, dogs and cats following episodes of uveitis. Alternatively, it can occur in certain breeds of dogs as a primary condition. These breeds include the Shih Tzu, Brussels Griffon, Chihuahua, Havanese, Italian greyhound, Lowchen, Papillon, Whippet and is seen occasionally in the Labrador retriever.

Why is vitreous degeneration significant?

Vitreous degeneration may be significant because it has been suggested that it may predispose patients to retinal detachment. Veterinary ophthalmologists are not certain about this, but from work that has been presented, it seems likely that vitreous degeneration is noticed in Shih Tzu dogs prior to retinal detachment. For this reason, patients found to have vitreous degeneration should be monitored for possible retinal detachment by the use of ultrasonography and careful examination of the retina at regular intervals.

If my pet is diagnosed with vitreous degeneration, what should I do?

Your pet may be diagnosed with vitreous degeneration during a routine ophthalmic examination or a breeding examination (C.E.R.F. examination). It is unlikely that a general veterinarian will find vitreous degeneration during an annual examination. If you have a pet which is in the breeds listed above, it is suggested that you have an ophthalmic examination or CERF examination by a veterinary ophthalmologist at some point in the future. Pets who develop retinal detachment in one eye should certainly have an ophthalmic examination.

What can be done if my pet has vitreous degeneration?

There are several viewpoints concerning what should be done. If your pet has not experienced retinal detachment, then regular examinations should be performed. If your pet has had retinal detachment, the Dr. Hacker feels that prophylactic lasering of the periphery of the retina should help prevent retinal detachment in the second eye.