Corneal dystrophy in a dog. How is a eyesore in a dog treated? Fatty degeneration of the cornea of \u200b\u200bthe eye in Siberian huskies

08.05.2020

Eye diseases have many negative consequences for the entire body. An ailment such as corneal dystrophy can lead to blindness, which will affect the quality of life of a pet. To avoid this, when the first symptoms appear, you should contact an ophthalmologist veterinarian who can prescribe adequate treatment.

Corneal dystrophy symptoms

Recognizing the disease is not so difficult. You just need to carefully monitor your pet. With corneal dystrophy in dogs, there is:

Discharge from the eyes and nose.
Blurred eyes.
Lachrymation.
Apathy.
Impaired coordination due to visual impairment.

To avoid further development of the disease, you need to make an appointment with a specialist as soon as possible.

What can be done at home to treat corneal dystrophy?

Provide peace.
Isolate from people and other pets.

Rinsing with saline is possible only as directed by a physician. Drops for humans are categorically not suitable for use in veterinary practice. The most correct decision of the owner will be to see a doctor.

How can a veterinarian help?

Initially, the doctor will conduct a diagnosis in order to confirm or deny the diagnosis. Although corneal dystrophy is common in dogs, treatment is individualized.

The veterinarian-ophthalmologist will carry out the necessary diagnostics, which includes:

Clinical examination.
Clinical tests: blood, urine and eye discharge.
Measurement of eye pressure.

In some cases, the disease can serve as a symptom of more serious pathologies of the body. A professional will always be able to figure out whether this is so - in a situation with your four-legged friend.

Types of treatment:

Medication.
In some cases, surgical.

Corneal dystrophy in dogs is difficult. The course is complicated by the fact that the pet cannot express its condition with words. A lot has to be guessed by indirect signs. By coming to our clinic, you can get rid of the disease forever. Experience and professionalism help our specialists to cope with even the most difficult cases.

Alexander Konstantinovsky, veterinarian, ophthalmologist, member of the board of directors of the European Society of Veterinary Ophthalmologists (ESVO)
Julia Nikolaeva, veterinarian, clinic "VetExpert", Kazan
The article uses photos by Alexander Konstantinovsky

Corneal dystrophies are hereditary diseases characterized most often by symmetrical lesions in both eyes. With dystrophies, various substances can be deposited in the cornea: lipids, cholesterol, calcium salts, etc. Clinically, dystrophy manifests itself as a local gray, white or metallic opacity on the cornea or in its thickness. The disease is more common in dogs, very rare in cats. Dystrophies usually debut at the age of 4 months to 13 years, they are not associated with eye and / or corneal injuries, with metabolism or with systemic diseases.

The cornea is a part of the outer membrane of the eye, normally it is transparent and does not contain blood vessels. The cornea in dogs and cats consists of four layers:

1) epithelium - the surface protective layer. Consists of several rows of cells, quickly renews and regenerates. The main function is to nourish and maintain optimal moisture in the cornea;

2) the corneal stroma - the most voluminous layer of the cornea, contains a large amount of collagen fibers. The upper layers of the stroma are very rich in nerve endings, therefore, with minor damage to the epithelium and irritation of these endings, the animal experiences severe pain and discomfort;

3) Descemet's membrane - separates the stroma from the endothelium. Has high elasticity;

4) the corneal endothelium - the inner layer of cells, which is involved in nutrition and is responsible for the transparency of the cornea. The endothelium is a kind of "pump" that pumps out excess fluid from the cornea. Does not regenerate in dogs and cats. In cases of damage to the endothelium, fluid from the anterior chamber begins to seep into the stroma, causing it to form vacuoles with fluid (bull).

Depending on the localization, epithelial, stromal and endothelial dystrophies are distinguished.

Epithelial dystrophies

With this type of dystrophy, the upper layer of the cornea is damaged. Violation of the corneal epithelium can be primary (the epithelial cells are damaged directly) or secondary (the corneal epithelium is damaged due to changes in the upper layers of the stroma). Clinically, these lesions are manifested by opacities, erosions and corneal ulcers. The animal experiences discomfort, corneal syndrome is observed (lacrimation, blepharospasm, photophobia). A distinctive feature of epithelial dystrophies is positive staining with fluorescein.

Treatment is most often ineffective, but there are a number of suggested surgical and therapeutic techniques. In therapeutic treatment, locally proteolysis inhibitors, antibacterial drugs and keratoprotectors are used. Surgery such animals can be performed superficial keratectomy. In the early postoperative period, this operation gives good results (the cornea becomes more transparent, there is no corneal syndrome), however, in the long-term periods, the recurrence rate is high. The disease can manifest itself as early as 4 months of age.

Affected breeds: Sheltie, Boxer, Pembroke Welsh Corgi, Boston Terrier.

Stromal dystrophies

This type of dystrophy is characterized by the deposition of lipids, cholesterol, calcium salts and other substances in the stroma. This condition does not bring any concern to the animal, it usually progresses rather slowly, and vision suffers slightly (although there are some exceptions).

Exposed breeds: Airedale, Dachshund, Afghan Hound, English Springer Spaniel, American Cocker Spaniel, German Shepherd, Basenji, Poodle, Beagle, Border Collie, Bichon Frize, Briard, Cavalier King Charles Spaniel, Irish Retriever wolfhound, labrador retriever, miniature pinscher, Scottish retriever, collie, samoyed, Siberian husky, alaskan malamute, lhasa apso, mastiff, pointer.

Among the predisposed breeds of Airedale terriers, stromal dystrophies have a specific course. In this breed, corneal dystrophy is sex-linked and manifests itself at the age of 4 months. The disease is characterized by rapid progression, leading to a significant impairment of vision up to blindness. Boston Terriers, Chihuahuas and Dachshunds can have a similar "malignant" course of degeneration.

This condition can be easily confused with non-hereditary diseases of another group - corneal degenerations. Corneal degeneration can result from a systemic disease in the animal (hypothyroidism) or from some previous corneal disorder. In this case, blood vessels may be present at the site of lipids, cholesterol, or metal salts.

Endothelial dystrophies

These dystrophies are characterized by damage to the inner layer of the cornea - the endothelium. This disease is similar to Fuchs's dystrophy, described in humans.

The pathogenesis is based on an increase in the permeability of the endothelium for fluid from the anterior chamber of the eye, which enters the corneal stroma and causes its edema (opacity). Endothelial failure can lead to keratitis bullous and secondary corneal ulceration. Bullous keratitis is a serious disease that is difficult to treat. Treatment options are discussed below.

Drug treatment

Hyperosmotic drugs (ointments and drops of 3-5% NaCl or KCl) are used to reduce corneal edema. The use of these drugs can reduce corneal swelling (usually for a short time), but in some cases the use of these drugs can be effective. long time (in these cases, hyperosmotic drugs are used for life). More effective way treatment is the use of soft contact lenses.

Surgery

In veterinary practice, the following are most often used:

Thermokeratotomy (penetrating keratoplasty);

Laser keratoplasty;

Conjunctival plastics;

Penetrating keratoplasty.

In medical practice, for the treatment of Fuchs's dystrophy, high-tech, complex techniques are used, which have recently found their application in veterinary medicine. It:

Deep lamellar endothelial keratoplasty;

Endothelial Keratoplasty with Descemet Membrane Removal (DSEK);

Descemet Membrane Transplant (DMEK).

Affected breeds: Boston Terrier, Chihuahua, Miniature Dachshund.

Conclusion

Corneal dystrophies are hereditary diseasestherefore it is not recommended to breed animals with epithelial, endothelial and "malignant" flowing stromal dystrophies. Animals with stromal lesions (in the absence of visual impairment) are undesirable for breeding.

SVM No. 4/2013

Muscular dystrophy in the Golden Retriever dog breed

Learn about Golden Retriever Muscular Dystrophy, a rare but deadly disease in dogs, and how MHDH helps treat Duchenne Muscular Dystrophy in humans.

Muscular dystrophy in dogs is more common in dog breeds golden retriever than other breeds; hence the name - Golden Retriever muscular dystrophy. MDHR is a degenerative muscle disease associated with a deficiency of the protein dystrophin. Although rare, this canine disease is severely crippling and ultimately fatal.

Since MGHR appears around the age of eight weeks, anyone planning to breed a dog, especially a Golden Retriever, or acquiring a puppy will benefit from additional knowledge of MGHR. There is no cure, but researchers have invented promising treatments for affected dogs, treatments that may also help treat the human form of MDHR known as Duchenne muscular dystrophy.

Which dogs are affected by Golden Retriever muscular dystrophy?

Golden Retriever muscular dystrophy usually occurs in purebred dogs, not exclusively in Golden Retrievers. But like Duchenne muscular dystrophy, MHDH occurs primarily in males. It is carried on the X chromosome, so a male Golden Retriever needs only one parent to pass on the defective gene, unlike a female Golden Retriever, which must inherit the gene from both parents. It is believed that female Golden Retrievers may be carriers of MGHR. They may also be diagnosed with the disease, but most females with MHDH develop light form disease. Fortunately, only a very small percentage of dogs - whether male or female, Golden Retrievers or others - are affected by MGHR.

Golden Retriever muscular dystrophy symptoms

The symptoms of MHDH are similar to those of Duchenne muscular dystrophy, but there are some differences. Symptoms in dogs with MHD: muscle weakness flexed state weakened walking difficulty swallowing excessive salivation problems chewing inverted feet shuffling gait difficulty breathing increased intolerance to walking

Prognosis and Treatment of Canine MHDH Disease

Dogs with severe Golden Retriever muscular dystrophy may not live longer than the first few days after diagnosis, but some dogs with the condition may survive for several years. Often the dog is killed by heart muscle disease caused by MGH. There is currently no proven effective treatment for MHDH. Despite this, there is some good news. Researchers at various institutes have studied gene therapy for MHDH with encouraging results. A 2006 study at the Stem Cell Research Institute in Milan found that affected dogs, with donor or genetically modified stem cells, showed an improvement in their symptoms. One dog could even run with a limp.

Later, researchers at the National Center for Neuralgia and Psychiatry in Japan had greater success with other gene therapy. They injected affected dogs with antisense molecules, creating DNA-like patches that cover the mutated patches and allow the dogs to make a functional version of dystrophin. What are the results? The injected dogs showed an improvement in muscle function and dystrophin production of 26 percent from normal levels.

Golden Retriever muscular dystrophy and Duchenne disease

Of course, these studies are much more important. By researching muscular dystrophy in dogs, experts believe boys with Duchenne muscular dystrophy can be helped with similar treatments - giving hope to Duchenne patients who often end up in wheelchairs and die in their teens or 20s.

Although it is necessary to conduct more research And experimentally, promising therapies may one day provide a cure for Golden Retriever muscular dystrophy and ultimately Duchenne muscular dystrophy. Meanwhile, genetic tests can recognize Golden Retrievers and other breeds that carry or are affected by MGHR.

To receive additional information For issues regarding Golden Retrievers, see Skin Problems in Golden Retrievers and Understanding Golden Retrievers.

Sources: Humphries, Courtney. "Fixing a Genetic Flaw." Technology Review (MIT), March 23, 2009. Associated Press. "Stem Cell Treatment Cures Muscular Dystrophy in Dogs." Foxnews.com, November 16, 2006 (accessed May 5, 2010). Coile, D. Caroline. The Golden Retriever Handbook. Hauppauge, NY: Barons, 2009.

Liver dystrophy (dystrorpiaperotis) - liver disease with severe dystrophic changes, with decomposition and resorption of the liver parenchyma.

Etiology. The main cause of liver dystrophy is intoxication of the body, which can be caused by spoiled food (acidified kitchen waste, spoiled fish and meat, etc.). The disease can be caused by poisoning with drugs of arsenic, phosphorus, mercury, organochlorine compounds.

As a secondary process, liver dystrophy can accompany gastroenteritis, demodicosis, salmonellosis.

Pathogenesis. Toxins that penetrate into the gastrointestinal tract or are formed in it are absorbed and enter the liver through the portal vein. Most often, the disease occurs in the form of fatty degeneration. Due to the violation of fat metabolism, many ketones, aldehydes, and low molecular weight acids are formed, which, having toxic substances, destroy fat-soluble vitamins, as well as some B vitamins present in feed.

Exo- and endotoxins disrupt the intracellular oxidative process, intrahepatic blood circulation is weakened, which leads to atrophy of hepatic cells.

Pathological changes. The surface of the liver is variegated, there is an alternation of areas of dark red, yellow and gray. The parenchyma is flabby, easily torn with fingers.

Clinical signs. Animals are oppressed, it is noted general weakness, stagnation. Body temperature is subnormal. Pulse and breathing are quickened. Tenderness to palpation in the abdominal cavity and symptoms of gastroenteritis. The yellowness of the mucous membranes is mild. Percussion and palpation in the region of the 10-13th rib causes a painful reaction. Oliguria is noted. The urine is dark green and frothy.

Diagnosis is put on the basis of anamnesis, clinical picture and laboratory tests.

Differentially, hepatitis and cirrhosis of the liver should be borne in mind.

Forecast must be careful. If the causes of the disease are not eliminated, animals die or cirrhosis of the liver develops.

Treatment start by eliminating the cause of the disease. The fat content of the diet is minimized and the intake of protein feed is limited. Be sure to do gastric lavage, and the intestinal tract is freed from the contents with enemas and laxatives (see Gastroenteritis). 5% glucose solution is injected subcutaneously in doses of 5-30 ml, insulin. Inside give ascorbic acid, cholasol (see. Hepatitis).

Prevention. It is necessary to protect animals from eating spoiled feed. Rodent baits containing poisonous substances should be laid out in places inaccessible to animals.

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The article will discuss pathologies corneas in dogs, in particular, pigment keratitis and corneal dystrophy. In veterinary medicine, the topic of eye diseases in dogs occupies a separate niche. Very often, these diseases are difficult to cure due to late diagnosis. After all, the owner of the animal cannot always recognize the signs of an incipient eye disease in a dog. For this reason, it is recommended that you visit your veterinarian regularly.

Corneal pathology

The general state of health of the cornea of \u200b\u200ba dog's eye is determined primarily by the degree of its transparency. Therefore, as soon as you notice clouding of the cornea in a dog, this may already indicate the presence of some pathology. The following signs also indicate the pathology of the cornea of \u200b\u200bthe eye:

bleeding in the eye;
swelling;
change in the color of the pupil;
calcium deposits (calcification);
inflammatory cell infiltrates;
destruction of enzymes by endogenous proteases of the body and, as a result, degradation and scarring of the cornea.

Such changes are abnormal and can be caused by various reasons... Pathogenetic reactions are often complex. Any pathology of the cornea of \u200b\u200bthe eye is a consequence, and the causative factor always lies in something else. It is this root cause that should be sought, and once discovered, every effort should be made for correct and thoughtful treatment and restoration of eye functions.

Superficial chronic keratitis in a dog

Superficial chronic keratitis (pannuses) is an immune-mediated keratitis, the cause of which should be sought in genetics, sometimes in the ecological situation of a particular region. The most favorable areas for the development of such a disease are places with an increased background radiation. If we talk about the influence of dog breed on the likelihood of chronic keratitis in a dog, then the most susceptible are German shepherds and their crosses. Greyhounds are also at risk. But most often dogs of all breeds suffer from chronic keratitis, and the statistical value among shepherd dogs and greyhounds is visible only when a large number of diseased individuals are studied. The disease begins with a slight symmetrical reddening of the cornea. Although it can start in other quadrants of the cornea and be asymmetrical.

Histologically, corneal infiltration is measured by plasma cells, lymphocytes, and blood vessels. As the process progresses, the entire cornea can be affected, which leads to a noticeable decrease in vision, and in the future - to blindness. Corneal opacity in a dog and proliferation of fibrous tissue (fibrosis) are characteristic signs of the chronic course of the process. The disease occurs at the age of 3-5 years. Pannus is very difficult to treat in young animals. Diagnosis is by clinical presentation, dog breed, and corneal or conjunctival cytology. Cytology usually shows elevated leukocyte and plasma cell counts.

Like most immune-mediated pathologies, chronic keratitis in a dog better to prevent than to cure. The complex of preventive measures includes the use of drugs of a number of corticosteroids, cyclosporins, Pimecrolimus (Elidel) and Tacrolimus (Protopic). The most preferred steroids are drugs with a content of prednisolone no more than 1% and dexamethasone (0.1%). The required frequency of medication is determined by the complexity of the dog's keratitis, the season and, on average, is about 2-4 times a day. Subconjunctival steroids can be administered as an adjunct to primary therapy or in particularly difficult cases. These drugs can be Triamcinalone, Methylprednisalone, or Betamethasone. They are all quite effective, however, for better removal of conjunctival formations, Betamethasone injections should be used. When treating keratitis in a dog local application of Cyclosporin at a concentration of 0.2%, 1%, 2% or Tacrolimus at a concentration of 0.02% or 0.03% is acceptable. Sometimes superficial chronic keratitis in a dog is treatable only when Cyclosporine or Tacrolimus are used alone. In some cases, the use of these drugs can reduce the use of steroids, which reduces side effects... Intensity treating keratitis in a dog can be reduced in the winter months and increased in the summer. Beta irradiation and plate keratectomy can act as additional treatment options, but today these technologies are practically not used. Plasma cells and lymphocytes are particularly sensitive to beta radiation, making ionizing radiation the most effective treatment for severe cases. However, the very strict licensing requirements for devices using strontium-90 have led to the fact that this method of treatment is almost never used.

Inflammation of the eyes in a dog (scleritis, episcleritis)

These are autoimmune and immune-mediated conditions that arise as a consequence of chronic infectious diseases, metabolic disorders or and are characterized by gradually spreading lesions of the sclera or episclera of the eye. Lesions can be unilateral or bilateral. Often only one quadrant is affected, and the neoplasm that appears is mistaken for scleritis. One way or another, a scleral neoplasm is different from melanoma. There is a genetic predisposition to this disease in Cocker Spaniels and Airedale Terriers. In Airedale terriers, the condition can often be complicated by the simultaneous development of uvitis (sclerovitis). Typical histological signs of scleritis and episcleritis in dogs may be the appearance of lymphocytes, plasma cells, and histiocytes in the sclera. The areas adjacent to the cornea of \u200b\u200bthe eye, as a rule, suffer from numerous microinflammations of blood vessels and tissues, and sometimes lipid degeneration is observed. Deep necrotic eye inflammation in a dog quite rare, but can cause serious intraocular disease (eg, retinal detachment). Diagnosis is clinical. A biopsy can be done, but this is often not a necessary procedure. Immune system tests are generally unhelpful and uninformative. Treating eye inflammation in dogs consists of a combination of the use of general and subconjunctival steroid drugs and anti-inflammatory nonsteroidal drugs. The latter include prednisolone, azathioprine, and the combination of tetracycline and niacinamide. In some cases, cyclosporine (both oral and topical) can be very effective. A long treatment period is expected.

Keratitis pigmentosa in dogs

Pigmentation of the epithelium of the cornea or its stroma is called pigmented keratitis (it is also sometimes called corneal melanosis or corneal pigmentation). Promote development pigmented keratitis in a dog there may be several factors, including a developmental disorder in the structure of the eye in the process of extraembryonic (placental) formation, excessive folds of the muzzle, dry eyes. Dry eyes are usually the most common cause of keratitis in most dog breeds (except pugs). Pigment overgrowth (pigmentation) can occur after a corneal ulcer (often post-traumatic) heals, or in parallel with another disease, such as pannus. A similar situation often occurs just with pugs. In this breed, genetically predisposed exophthalmos and corneal exposures can be provoking factors. In any case, the most important factor for the development of such a pathology is the breed of the dog, since, despite the similar structure of the head structure, pigment keratitis is much less common in dogs of such breeds as the Bulldog, Pekingese and Shih Tzu. Cantoplasty and cantopexy (lower eyelid lift) are often used to slow the progression of the disease. The advantage of this procedure is to increase eye protection by reducing the palpebral fissure, eliminating trichiasis (abnormal growth) of the nasal hairs and correcting the canthal ligaments of the inner and outer corners of the palpebral fissure, as well as nasal skin folds.

For pugs, a comprehensive treatment approach is used pigmented keratitis, combining surgery and local treatment at the same time. Local treatment can slow down painful inflammatory processes and consists of the use of drugs cyclosporine, tacrolimus and corticosteroids. Cyclosporine and tacrolimus are approximately the same in their effectiveness and the final choice depends only on which drug is best suited for a particular patient. Steroid use can only be beneficial in the case of brachycephalic breeds of dogs, due to their tendency to corneal ulcers. It is also sometimes permissible to use beta-irradiation, but it is justified only in cases where vision is significantly affected and melanotic germination is significant, in other cases, the use of this type of treatment is impractical.

Endothelial corneal dystrophy in a dog

Such a pathology is primarily caused by a defect in the corneal endothelium, which leads to its edema and, in the future, gives the cornea a bluish-gray tint. Primary causes in the differential diagnosis of edema, you can consider corneal ulcers, uvitis, glaucoma, which are easy to distinguish and recognize by their condition. Endothelial corneal degeneration in a dog progresses slowly and usually begins in the lateral part of the cornea, but then spreads to its entire area. Breeds such as the Boston Terrier and Chihuahua are most likely to have this disease, but dogs of all breeds are often affected. At an early stage, the disease usually does not cause painful conditions in the patient. Developing and progressive endothelial corneal dystrophy causes ulcerative keratitis and pain over time.

Therapy consists mainly in the application of 5% sodium chloride ointment or suspension (Muro-128) to minimize swelling. In any case, a sufficiently quick cleaning of the cornea of \u200b\u200bthe dog's eye should not and should not be expected. Local antibiotics or atropine are used only in cases of corneal ulcers in a dog... Conjunctive hyperemia occurs in an already ill dog. If the eyes are particularly irritated and there are no ulcers, topical steroids can be used with caution. Local non-steroidal anti-inflammatory drugs (Flurbiprofan) are also successfully used in some cases. Thermal moxibustion (thermokeratoplasty) is used in especially severe cases and when corneal ulcers are opened. This procedure, although it will not clear dog cornea completely, but will prevent swelling and ease the pain experienced during the opening of ulcers. The essence of this technique is to use an ophthalmic laser to cauterize damaged areas of the cornea. It should be noted that the success of the operation depends on the skill of the surgeon, since inaccurate movement or too long burning can lead to the complete destruction of the cornea of \u200b\u200bthe dog's eye. Also, in some cases, it is advisable to use penetrating keratoplasty.

Lipid or calcium keratopathy in dogs

Deposition of lipids and salts on the cornea of \u200b\u200bthe eye in a dog are quite similar to the diseases described above, but have completely different causes, and their clinical differences are sometimes difficult to distinguish. However, there are three main signs by which pathological corneal deposits can be diagnosed:

corneal dystrophy in a dog;
degeneration of the cornea of \u200b\u200bthe eye;
lipoid arch of the cornea (grayish line at the periphery of the cornea, a kind of annular opacity of the periphery, separated from its other parts).

Corneal dystrophy in dogs can be: hereditary, bilateral, symmetrical. There are also cases when dystrophy begins to progress in one eye, and then spreads to both. Corneal lipid dystrophy can occur in different breeds of dogs, however, Siberian huskies, Samoyeds, cocker spaniels and beagles are more often at risk. Clinically, lipid deposits can create a light, almost imperceptible crystalline fog in the central part of the cornea, or the affected part of the cornea can be completely opaque. Lipid deposition is usually subepithelial or stromal and consists of cholesterol, neutral fats, and phospholipids. There is no systemic character in this disease and, as a rule, is not observed. The cornea is usually without ulcers and there is no inflammation. Very rarely, lipid deposits worsen dog sight, however, they also do not cause painful sensations. For these reasons, dogs are not prescribed any specific treatment for such a pathology. If the treatment begins, then lamellar keratectomy is used, however, it does not guarantee the repetition of deposits, and the reason for this is persistent disorders of lipid metabolism in the parenchyma leading to new and new germinations.

Degeneration of the cornea of \u200b\u200bthe dog's eye can be caused by both lipid and salt deposits (and sometimes both). Initially, degeneration can be preceded by canine corneal ulcers, uvitis and sometimes exophthalmos. Unlike corneal dystrophy, degeneration is more often unilateral than symmetrical (bilateral). The affected part of the cornea, most often, is opaque, rough, with destroyed epithelium. And this already creates some discomfort for the animal. Inflammation, vascularization and pigmentation may also occur. As a treatment for degeneration of the dog's eye, the same lamellar keratectomy - it allows you to reduce pain, restore vision, but with all this, this treatment does not guarantee the avoidance of relapse. In some cases, it is useful to use the ointment in conjunction with keratectomy. An alternative to the operation is the long-term use of abrasive and at the same time resolving agents, such as powdered sugar, preparations based on natural honey and propolis, various combinations of bee bread, wax and bee pollen. Be sure to use them simultaneously with ointments and drops without corticosteroids. However, their use (they are less traumatic) and their effectiveness have not yet been sufficiently studied, and are only a weak alternative. modern methods and recovery approaches dog vision.

Corneal lipid degeneration can occur after a long period of treatment with corticosteroids, such as cataract surgery, but such degeneration is not difficult to treat. Degeneration may regress after several treatments.

The deposition of lipids that occurs in the periphery of the cornea, in combination with persistent hyperlipidymia, is called the lipoid arch of the cornea (annular opacification of the periphery of the cornea). Clinically, fat creates an opaque ring in the periphery of the cornea. Any breed of dog can have a problem, but German Shepherds are particularly susceptible. Annular opacity of the corneal periphery is a bilateral problem and is accompanied by mild inflammation and vascularization. Treatment is solely aimed at eliminating the underlying factor. In dogs suffering from lipid and salt deposits, the first step is to take a blood test to check the level of cholesterol, triglycerides, and also examine the thyroid gland. If the test results are satisfactory, then the dog's diet should be changed and this will partially solve the problem of lipid deposits.

Punctate keratitis in dogs

Punctate keratitis quite rare in dogs. Note that most often dachshunds are sick with it. Punctate keratitis is of an immune-mediated nature of origin and is a particular form of corneal ulceration. On the cornea affected by punctate keratitis, punctate clouding of the cornea of \u200b\u200bthe eye in a dog in the form of small fluorescent spots. Punctate keratitis affects one or both eyes. Topical application of cyclosporine in the form of drops or ointment may help, but concurrent topical steroids will be more effective.

Sheltie corneal dystrophy

A similar disease occurs in the Sheltie and sometimes in the Collie, but the cause is still not fully understood. Many dogs have multifocal corneal opacities with persistent fluorescence. Secondary corneal degeneration may occur. The disease is very similar to punctate keratitis and is treated by the same method. However, topical application of steroids must be carried out very carefully, since the reaction of the animal to the drug is sometimes difficult to predict. In the affected eye with dystrophy of this kind, a small amount of tears are produced, which leads to an aggravation of the process ("vicious circle").

Corneal neoplasms in dogs

Tumors of the cornea of \u200b\u200bthe eye in a dog occur quite rarely. The most famous are dermoid and lumbar melanomas. Dermoids are benign congenital neoplasms that are most often observed on the temporary cornea. They are quite easy to remove with a plate keratectomy... Lumbar melanomas histological signs - malignant tumors, however, they develop as benign. Their growth is very slow, however, if you ignore them for a long time, they will fill all the space available to them. From their classification name, it is clear that they are formed in the corneoscleral junctions (limbs). Surgical treatment significantly slows down the progress of the disease. However, during the operation, the eye can be damaged too much, which indicates the doubtfulness of this method of treatment. Surgical intervention is understood as either complete excision followed by inoculation, or partial removal followed by laser correction.

Spontaneous Chronic Corneal Epithelial Defects in Dogs

This is a particularly unpleasant disease (in terms of diagnosis and treatment) for veterinary medicine specialists, which is a specific ulcerative process. Usually, these processes are chronic, superficial, non-infectious (with the exception of feline herpes) and practically painless. In most cases, there is excessive stratification of the corneal epithelium and variable vascularization. Ulcers form abnormalities of the corneal epithelium and basement membrane. All dog breeds are affected. Most often, dogs of middle and old age are affected. Appropriate topical treatment should include antibiotics and atropine 1% once or twice daily. To reduce the likelihood of relapse, topically apply ointment or drops of sodium chloride. Also, topical application of cyclosporine reduces the likelihood of scarring. Surgery and grid keratomy (mesh keratotomy) are often recommended for complete healing. The aim of the procedures is to restore the basement membrane and improve the connection between the epithelium and the stroma.

Mesh keratotomy

This procedure is only intended to treat superficial non-infected ulcers and should never be applied to deep corneal ulcers. Mesh keratotomy performed after preliminary surgical treatmentas described above. General anesthesia is recommended for restless dogs or when the operation is performed for the first time. In other cases, mild sedatives are sufficient. Needles, 22 or 25 in diameter, are used for superficial cuts in the form of a mesh. The mesh is created by "tracing" the needle over the cornea, with an inclination of 30-45 °. Deep penetration into the cornea should be avoided. Otherwise, continue with the prescribed treatment. Anti-inflammatory analgesics are used after the procedure (for example, non-steroidal analgesics and tramadol). It is recommended that the dog wear a protective Elizabethan collar immediately after the operation. Most ulcers heal within two weeks after the mesh keratotomy procedure.

Lipoid (fatty) corneal degeneration in dogs is the deposition of lipids in the corneal stroma, resulting in a white or white-gray patch on the cornea.

Fatty degeneration of the cornea may be primary or secondary to other ocular diseases. One or both eyes may be affected.

The reasons

A hereditary pedigree predisposition to corneal fatty degeneration was revealed: Siberian huskies, beagles, American cocker spaniels, cavalier king charles spaniels, and German shepherds are at risk. Both eyes are usually affected and the cause of lipid deposition in the cornea remains unknown.

Also, the disease can develop against the background of hypothyroidism and concomitant high blood cholesterol.

Inflammatory eye diseases (dry eye syndrome, uveitis, pannus, etc.) can lead to the development of corneal lipoid dystrophy.

Signs

The disease leads to a violation of the transparency of the cornea. Opacities appear on it, spots of white or gray color, vascularization (germination of blood vessels) occurs. Pigmentation (dark discoloration) of the cornea may appear.

Sometimes the disease develops against the background of dry eye syndrome - in this case, dryness and inflammation of the cornea (keratoconjunctivitis dry) is noted. You can also see signs of other inflammatory eye diseases: redness, discharge, tissue edema, squinting eyes, photophobia, clouding of the anterior chamber of the eye.

Diagnostics

A complete physical examination of the patient is performed. As a rule, a general clinical blood test is within normal limits. In a biochemical blood test, an increase in cholesterol levels is possible. Blood tests for thyroid hormones may be ordered.

A complete ophthalmological examination is performed, including the Schirmer test to exclude dry eye syndrome, a fluorescein test to detect corneal damage, eyelid examination, and examination of the internal structures of the eye.

Treatment

Fatty degeneration (lipidosis) of the liver - It is a non-inflammatory disease of the parenchyma (the main functional cells, i.e. hepatocytes) of the liver, associated with metabolic disorders in the animal's body. Since the liver takes an active part in the metabolism of fats, the violation of this metabolism leads to the accumulation of fatty deposits in hepatocytes.

Pathophysiology.

Fats from food are broken down in the intestine with the help of pancreatic enzymes and absorbed into the bloodstream. From there they enter the liver, where they are converted into various substances of intermediate metabolism of fats: triglycerides, cholesterol, phospholipids, etc. Fatty infiltration of the liver occurs in the case of accumulation of a large amount of triglycerides in it (more than 50% of the liver mass, at normal - no more than 5%) ... The factors leading to this condition are varied: increased intake of fatty acids from food, increased formation of triglycerides in the liver, impaired transport of triglycerides from the liver to adipose tissue, where they are normally deposited.

Causes of the disease:

Castration of animals, i.e. removal of the sex glands.

In the modern world of cities and megalopolises, cats and dogs have ceased to be predators. Animals kept in apartments of cities are delicate and capricious. For the convenience of owners and the health of pets, animals are often castrated, after which they become more calm and apathetic, their lifestyle changes. They eat a lot and move little, which leads to the accumulation of fat in the body.

In addition, the removal of the sex glands itself affects fat metabolism, due to changes in hormonal balance. Sex hormones affect the level of feed intake and body weight, directly affecting the central nervous system, or indirectly, by altering cellular metabolism. Estrogens limit the need for feed, so during estrus it decreases markedly. This does not happen after castration. Deficiency of estrogen plays a major role in the dysregulation of metabolism, including fats. Estrogens have a direct effect on lipogenesis in the body and determine the number of fat cells in cats. Neutered cats are more prone to obesity and liver lipidosis than neutered cats. Sterilized and neutered dogs are less likely to suffer from this disease.

in the stage of decompensation. If glucose metabolism is impaired in the liver, a violation of the deposition of fatty substances may occur. And, conversely, with liver lipidosis, a violation of its structure and function occurs, the level of the hormone insulin increases. Type 2 diabetes in cats is associated specifically with obesity and fat accumulation in hepatocytes.

One of the most common disorders of fat metabolism with excessive accumulation of fat in the liver against the background of a lack of carbohydrates is ketosis - increased formation of ketone bodies as a result of impaired metabolism and their accumulation in tissues in decompensated type 2 diabetes mellitus.

Fatty hepatosis develops with a deficiency of enzymes that break down fats, for example, with exocrine pancreatic insufficiencyand etc.
Overfeeding and increased intake of fat from food. (High fat feed with natural feeding type)
Protein deficiency (The accumulation of fat in the liver is associated with an insufficient amount of protein and impaired transport of fat from the liver to the tissues).
Poisoning with hepatotropic poisons (carbon tetrachloride, DDT, yellow phosphorus, etc.).
The use of certain drugs.
Fatty liver disease is often combined with dyskinesia (violation of tone) of the gallbladder, especially with gallstone disease.

Depending on the nature of fat deposition, fatty degeneration of the liver is divided into large-droplet and small-droplet (the size of fat droplets in liver cells). Depending on the nature of the flow on acute and chronic process.

Clinical signs.

The course of the disease is erased, slowly progressing. Cats can live with fatty infiltration for a long time, but any stress factor can lead to the manifestation of the clinical picture of lipidosis. Stress can be of any etiology - moving, deteriorating living conditions, a sudden change in food, the appearance of other animals or children in the house. At the same time, cats simply refuse to take food and begin to lose weight dramatically, which aggravates the course of the disease. Animals become lethargic, lethargic, blood glucose rises (secondary diabetes mellitus), which is accompanied by an increase in water consumption () and urinary volume (polyuria). Over time, there may be nausea, vomiting, stool disturbances. Jaundice and abdominal pain are rarely detected. Examination reveals an enlarged liver, less often tension in the abdominal wall (which in animals indicates pain).

Diagnostics.

Includes clinical examination and palpation of the abdominal wall, blood tests, ultrasound and radiography of the abdominal organs.

Fatty degeneration of the liver clinically, as a rule, rarely manifests itself and in cases of a long-term illness. Fatty degeneration can be suspected by enlargement of the liver in size with palpation of the abdomen. Liver enlargement is confirmed with Abdominal ultrasound, but an accurate diagnosis based on the results of ultrasound with this pathology cannot be established. Confirming the presence of lipidosis is possible only when histological examination liver tissue and detection in hepatocytes by microscopy of the accumulation of fatty vacuoles.

This requires a biopsy of the liver tissue under ultrasound control, or intraoperatively. It is also possible to confirm the diagnosis with CT or MRI examinations. There are 3 degrees of liver lipidosis, depending on the amount of affected liver tissue.

Laboratory diagnosticsincludes a biochemical blood test that helps to identify the abnormalities that caused the disease.

Treatment.

Treatment tactics depend on the cause of the disease. Proper nutrition, correction of metabolic disorders, as a rule, lead to an improvement in the condition. Prescribe a diet with increased content proteins, limiting fats, especially animal origin.

However, food refusal is a leading complication of liver lipidosis in cats. In this case, the animals must be force-fed, most often using a nasoesophageal tube or parenteral nutrition. This is carried out only in a hospital setting veterinary clinic... Force feeding should ensure that the animals receive sufficient energy and nutrients... It is advisable to determine the level of energy and nutrient intake for each patient individually, taking into account the degree of liver damage and the tolerance of the protein contained in the diet.

In addition, the animal needs a comprehensive infusion therapy, in order to prevent dehydration of the body, the use of a complex of medications that support and restore liver function, as well as in symptomatic therapy that stabilizes the condition of the animal.

If your pet is overweight, and even more so, obese, be as careful as possible about the health of your pet. Do not expose him to unnecessary stress, do not let him lose weight dramatically. If there is a refusal to feed, or a decrease in appetite, lethargy and apathy, you should not wait more than a day, you need to seek help from veterinary specialists as soon as possible, carry out the necessary research and provide all help needed animal.

If treatment is started on time, there is always a chance to maintain the proper level of quality of life for a pet with a pathology such as liver lipidosis. However, it should be borne in mind that the structure of the liver will never be fully restored and these changes are likely to persist until the end of the animal's life.

Corneal dystrophy is a hereditary pathology in which substances that impair its transparency are deposited into the cornea. Pathology always symmetrically manifests itself in both eyes in the form of round / oval white-gray opalescent spots in the central part of the cornea. Both eyes can be affected at the same time, or with a little difference in time: first one, and after a while the second eye. The area, depth, and intensity of the lesion vary from animal to animal.

In most cases of corneal degeneration, cholesterol / phospholipids / fatty acids / calcium salts are deposited in the stromal layer, just below the epithelium. This is a painless process, but as it progresses, the amount of deposits will increase, which can provoke corneal ulceration. The more deposits, the more deteriorating vision.

Corneal dystrophy in a dog, right eye Corneal dystrophy in a dog, left eye

Diagnosis of corneal dystrophy in dogs and cats.

A patient with suspected corneal dystrophy needs an ophthalmologic examination. Based on the results of the examination, additional studies may be prescribed for Cushing's syndrome, hyperthyroidism, hyperlipoproteinemia, diabetes mellitus.

Differential diagnostics.

Corneal lipidosis, corneal degeneration, corneal edema.

Corneal dystrophy treatment.

Since the process is genetically determined, there is no specific and effective treatment. Sometimes the process progresses more strongly with improper feeding (an excess of fat in the diet). In this case, the patient is advised to correct the diet. In the event that the deposits began to provoke corneal ulceration, the patient begins to experience painful sensations. Pain syndrome develops (blepharospasm, lacrimation, redness of the eye). This condition is an indication for superficial keratectomy. During this surgery, the dystrophy zone is removed, and the cornea regains its transparency. Treatment is temporary, since corneal dystrophy will develop again in the same place in the future. However, this is a rather lengthy process and can take from several months to a year. In the event that ulceration develops again, a repeated keratectomy is performed.

An alternative surgical treatment may be keratotomy with a diamond bur, which has proven itself to be excellent in the treatment of this disease. Recently, more and more of my patients are being treated and cured with this method. Unlike surgery, it is performed without general anesthesia, which significantly increases the relevance of the procedure. Since this procedure may have contraindications, an in-person consultation with a veterinarian and an ophthalmologist is required before performing a keratotomy with a diamond bur.

Ulceration in corneal dystrophy Positive fluorescein staining

Predisposed dog breeds.

The disease can manifest itself in any dog, cat, but more often than others, this disease is diagnosed in the following:

The etiology of non-ulcer corneal lesions is diverse. In the normal state, the cornea is transparent due to its non-keratinized epithelium, the clear organization of thin collagen fibers, the pulsation of the epithelium, and the absence of blood vessels and pigment. Corneal pathological reactions can be various combinations of edema, vascularization, pigmentation, accumulation of cellular and metabolic (lipids and minerals) infiltrates, fibrosis and ulceration. These changes can lead to corneal opacity and visual impairment.

The main diseases that occur without corneal ulceration are keratoconjunctivitis dry (see the article of the same name earlier), chronic superficial keratitis, pigmentary keratitis, corneal dystrophy, corneal degeneration, lipid keratopathy, nodular granulomatous episklerokeratus rheumatoiditis, sequesteritis infection. Dry creatoconjunctivitis and herpesvirus stromal keratitis have already been described in relevant articles.

Chronic superficial keratitis (pannus)

Chronic superficial keratitis (COD), or pannus, is a bilateral, progressive, impaired, mostly non-ulcerative, inflammatory disease that usually begins in the lateral and ventrolateral cornea. The third eyelid can also be affected, both simultaneously and separately (atypical pannus). COD is characterized by vascularization of the corneal surface, pigmentation and infiltration by lymphocytes and plasma cells. If untreated, permanent blindness can occur due to continuous pigmentation. COD is most common in German Shepherds, but dogs of any breed can be affected. Increased morbidity has been reported in Belgian Tervuren, Border Collie, Greyhound, Siberian Husky and Australian Shepherd. Most often, dogs get sick in middle age. Although the exact etiology is unknown, an immune-mediated mechanism of the disease has been suggested, and ultraviolet radiation may also play a role in the pathogenesis of COD. Prolonged exposure to ultraviolet rays increases the incidence and severity of pannus.

COD is tentatively diagnosed based on clinical symptoms. But first, it is necessary to exclude constant irritation (with dry keratoconjunctivitis, entropion, lagophthalmos) as the cause of increased vascularization and pigmentation. Tear production should be assessed and a thorough eye examination performed, with particular attention paid to the structure of the eyelids. The diagnosis of COD is facilitated by cytological analyzes of ocular abnormalities, especially if they contain many lymphocytes and plasma cells.

The goal of therapy is to control rather than cure the disease. Life-long treatment should be considered, but aggressive medication may be required during the winter. The main agents of drug therapy are corticosteroids and / or cyclosporine (Optimmun, Schering-PljughAnimalHeath).The severity of the disease varies greatly, therefore, the treatment is selected individually. In severe cases (negative results of fluorescein staining), subconjunctival injections of 4-6 mg of triamcinolone are performed (Vetalog, SolvayAnimalHealth) or 1 mg dexamethasone (Asium, Schering-PljughAnimalHealth) during diagnosis or on demand. All cases that we observed were small or moderate, therefore, we prefer to start treatment with cyclosporin ointment every 12 hours and a 1% suspension of prednisolone acetate (Econopred Plus, Akop) every 6-12 hours. Alternatively, dexamethasone (Maxidex, Akop) can be used instead of prednisolone acetate. The author prefers to use one of these corticosteroids because they are stronger and penetrate the cornea better than others. The aim of therapy is to reduce the infiltration of inflammatory cells and vascularization of the cornea, as well as to prevent the progression of corneal pigmentation. As a result of treatment, corneal opacity should also decrease, and vision should improve. When the clinical symptoms are under the control of drug therapy, the dosage is gradually reduced to the minimum that can ensure the satisfactory condition of the animal. Reevaluation of patients with COD is urgently needed because changes in drug treatment need to be made due to variations in disease progression.

In cases that are not amenable to drug treatment, or with severe pigmentation, superficial keratectomy and beta-irradiation are performed, but drug therapy is continued in parallel. Beta irradiation is non-invasive and strongly reduces superficial pigmentation within 3-6 weeks. Cryosurgery using liquid nitrogen and nitric oxide can also reduce superficial pigmentation over several weeks and improve vision.

Pigmented keratitis

Pigmented keratitis is characterized by pigmentation of the corneal epithelium and subepithelial stroma. It can be accompanied by varying degrees of superficial vascularization. Corneal pigmentation is a nonspecific response to persistent irritation caused by a variety of causes, including keratoconjunctivitis dry and abnormal eyelids. The fundamental point of treatment for this disease is to determine the root cause. Keratoconjunctivitis dry is defined as a disruption in the normal production of tears. This section discusses the keratitis pigmentosa that is caused by persistent irritation due to structural abnormalities such as entropion, distichiasis, nasal fold trichiasis, and lagophthalmos (incomplete eyelid closure). The most severe cases occur in dogs with a large palpebral fissure, lagophthalmos, entropion of the medial lower eyelid and nasal trichiasis (Pugs and Pekingese). Keratitis pigmentosa is especially common in brachycephalic dog breeds. They can suffer from strong visual compromise due to extensive diffuse corneal pigmentation.

The key to correct treatment pigmentary keratitis is the early diagnosis of corneal pigmentation and recognition of the predisposing causes. The disease is best prevented by prevention, excluding these causes. The main treatment is surgical correction of any structural anomalies, which may include resection of nasal folds, entropion correction, or medial cantoplasty. Most brachycephalic dogs benefit from medial cantoplasty, which eliminates lagophthalmos and entropion of the medial lower eyelid. Medial (or medial and lateral) cantoplasty is many times more effective than lateral cantoplasty in reducing clinical symptoms, which are mainly caused by nasal trichiasis.

In many cases, pigmentation is already present to varying degrees at the time of diagnosis. Removing existing pigmentation is an unrealistic goal. The aim of the therapy is to prevent the progression of the corneal pigmentation leading to blindness. In addition to treating the underlying problem, cyclosporine can be given every 12 hours in an attempt to reduce pigmentation density. With very strong pigmentation, surgery may be considered only if the underlying cause has already been ruled out (otherwise the pigmentation will reappear). Beta irradiation, lamellar keratectomy and cryosurgery are used to reduce pigmentation.

Corneal dystrophy

Corneal dystrophy is much more common in dogs than in cats. In dogs, it is classified according to the anatomical location of the disorder - epithelial, stromal, or endothelial. Feline corneal dystrophy has been reported in tailless and shorthaired cats. Several cases of corneal stromal and / or endothelial disease followed by severe stromal edema have been described.

Epithelial dystrophy
The most common form of corneal dystrophy is actually dystrophy of the basal epithelial membrane, which is most commonly seen in boxers but can also occur in other dog breeds. Slow healing ulcers are a manifestation of this disorder, which are discussed in various articles in this book.

Stromal dystrophy
Corneal stromal dystrophy is primary diseaseusually a bilateral, predominantly hereditary condition of the cornea that is not due to systemic or inflammatory diseases... Corneal stromal dystrophy most often begins in young or middle-aged dogs. The clinical symptom is a white, crystalline corneal opacification called "gray glass". The lesion is usually well-defined and centered or near the center of the cornea, usually round, oval, or annular in shape.

Corneal opacity is caused by extracellular and intracellular deposits of phospholipids, neutral fats and cholesterol in the superficial or deep corneal stroma, localization clearly depends on the breed of the affected animal. Lipid deposits are most often localized subepithelially, the overlying epithelium usually remains intact, therefore, in this disease, the results of fluorescein staining are usually negative. Although corneal dystrophy can occur in all breeds of dogs, there are several forms of corneal dystrophy that will be specific to certain breeds, such as the Siberian Husky, Beagle, Scottish Shepherd, and Cavalier King Charles Spaniel.

A preliminary diagnosis is made based on the above symptoms. The main point of the differential diagnosis is lipid deposits in the cornea after systemic hyperlipidemia, therefore, a biochemical analysis of serum (including the concentration of cholesterol and triglycerides) should be included in the diatostics plan, especially in atypical cases.

Although there is no effective medical treatment for corneal dystrophy, the disorder is usually painless and permanent. Corneal opacities can be removed with superficial keratectomy, especially if they interfere with vision. The result will be some scarring and there is also the potential for relapse. Keratectomy requires augmentation, special instrumentation designed for operations on the cornea, and a certain level of surgical skill at the performer, because the thickness of the cornea is on average 1 mm and a full-layer corneal incision can be easily made.

Endothelial dystrophy
Most often, endothelial dystrophy occurs in middle or old age in Boston Terriers, Chihuahuas and Dachshunds, but the disease can also occur in any other breed of dog. Endothelial dystrophy leads to a decrease in the number of functioning endothelial cells. Since the most important function of the corneal endothelium is to actively pump fluid out of the cornea to maintain its turgor, the clinical result of endothelial dysfunction will be corneal edema (first stromal, then epithelial). Corneal edema in endothelial dystrophy is usually diffuse (homogeneous light blue color of the cornea), it progresses and inevitably ends in blindness. Corneal edema begins in the temporal part of the eye and then progresses linearly. With severe corneal edema, vesicles form in the epithelium and subepithelium, which burst and give rise to corneal ulcers. In severe cases of endothelial dystrophy, especially with corneal ulcers, corneal vascularization may also develop. This type of corneal ulcer heals very slowly due to the persistence of the underlying disorder, and lattice keratectomy must be performed to heal.

There is no effective drug treatment for endothelial dystrophy. If corneal ulcers are the result of ruptured vesicles, they should be treated with topical antibiotics. Recurrent corneal ulcers are treated with soft contact lenses or lattice keratectomy. Some veterinarians prefer to treat corneal edema with topical hyperosmotic drugs, such as 5% sodium chloride ointment. (Muro 128, Bausch & Lomb). In theory, it should create an osmotic gradient in the cornea and facilitate the movement of fluid out of the cornea, thereby relieving swelling and reducing vesicles. However, the relief of edema is usually minimal, and some animals develop eye irritation.

For animals with severe corneal edema due to endothelial dystrophy or recurrent corneal ulcers due to rupture of epithelial and subepithelial vesicles, surgery should be considered. One of the methods is penetrating keratoplasty (corneal graft), but rejection of the graft leads to clouding of the donor cornea, thus, vision may not be restored. Thermocauteroplasty is a careful and controlled application of a thermocauter to the cornea in order to induce the formation of a surface layer of fibrous tissue. The meaning of this procedure is to reduce or stop the release of edematous fluid into the corneal epithelium and, accordingly, to prevent the formation of corneal vesicles and subsequent corneal ulcers.

Corneal degeneration

Corneal degeneration consists of stromal deposits of lipids (sometimes called lipid keratopathy), cholesterol, or calcium. This process can be accompanied by vascularization. Degenerative disorders are usually white and crystalline in appearance. Most often they form in the center of the cornea, but depending on the reasons, they can be in other places. Sometimes these disorders can be accompanied by ulcers of the overlying epithelium.

Corneal degeneration can result from corneal trauma, ulceration, persistent irritation, uveitis, and topical corticosteroid therapy. Degeneration can also result from hyperlipidemia and hypercalcemia. Corneal degeneration can be unilateral (most commonly) and bilateral in contrast to corneal degeneration, which is typically bilateral.

Calcium degeneration (ribbon-like keratopathy) may result from impaired systemic calcium and phosphorus metabolism and has been reported in dogs with hyperadrenocorticism. Infiltration of lipids into the cornea can be caused by systemic hyperlipidemia due to hypothyroidism, diabetes mellitus, hyperadrenocorticism, pancreatitis, nephrotic syndrome, liver disease, or primary hyperlipoproteinemia (in miniature schnauzers). The diagnostic plan should include a biochemical analysis of blood serum, including cholesterol and triglycerides, and, possibly, determination of the concentration of thyroid hormones.

If the eye sees and there is no discomfort in it, then no treatment is required, but control of all the main causes of the disease is necessary. In the case of calcium degeneration, drug therapy should be prescribed to reduce the amount of mineral infiltrates into the cornea. A topical solution of disodium ethylenediaminetetraacetic acid (EDTA) (0.4 or 1.38%) is given every 6-8 hours to chelate calcium from degenerative disorders and reduce their density. For cholesterol and lipid deposits, a fat-free diet is recommended. Although the response to treatment is usually unpredictable, especially in the absence of hyperlipidemia, improvements in corneal health have been noted despite no decrease in serum cholesterol and triglyceride concentrations.

In problematic cases (visual impairment, corneal ulcer or eye irritation), degenerative corneal disorders are surgically removed by performing a keratectomy. Corneal specimens should be subjected to histopathological analyzes, including special staining for calcium and lipids. This procedure is carried out only if the underlying cause is under control, otherwise relapses of the disease are possible.

Arcus lipoides corneae (senile arc)

Arcuslipoid.escoteae (senile arch) is a bilateral disorder caused by the deposition of lipids in the corneal stroma, characterized by the formation of an arch around the limbus of the cornea. Lipid deposition begins in the deep stromal layers, and then inevitably involves the surface layers. These can be thin, transparent areas between the limbus and the outer edge of the arch. The senile arch most often accompanies hypothyroidism, but can be the result of any disease that causes an increase in the concentration of cholesterol and triglycerides in the blood. Treatment should be directed to the underlying cause (prescription of thyroid hormones in hypothyroidism).

Nodular granulomatous episcleritis

Nodular granulomatous episcleritis (NGE) is an inflammatory, nodular disorder of the corneal-scleral limbus. Other names for this disease are fibrous histiocytoma, nodular fasciitis, pseudotumor, and collie granuloma. It is believed that all these are different histological manifestations of one underlying disease. Histological analyzes show that the contents of the nodules around the limbus vary in the content of lymphocytes, plasma cells, histocytes and fibroblasts.

Nodular granulomatous episcleritis may be unilateral, but it is mostly bilateral; there may be more than one nodule in one eye. Young or medium-sized dogs are most commonly affected.
age. The exact etiology is unknown, but an immune-mediated mechanism is most likely. Disorders most often develop on the lateral part of the limbus, if untreated, they slowly progress and gradually invade the corneal stroma (and, therefore, impair vision if left untreated). They are characterized by a high rate of local recurrence in the absence of appropriate treatment. The abnormalities typically appear as growing, smooth and pink nodules in the limbus of the cornea. There may be parallel involvement of the third eyelid or eyelids. The most susceptible breed is the collie, the lesser incidence is observed among the Sheltie, but the disease occurs in dogs of all breeds.

The diagnosis is based on the results of cytological examination of the mass obtained by a biopsy with a fine needle, or a biopsy of the lesion. For diagnostic and therapeutic purposes, keratectomy can be performed, but additional drug therapy is needed. Ideally, at the onset of the disease, histological confirmation of the preliminary diagnosis is needed, or these tests are performed in the absence of a response to drug treatment. The differential diagnosis includes neoplasia and infection, but these are unlikely.

Drug therapy for this disease is based on corticosteroids alone or in combination with azathioprine. In mild cases, therapy is started with 1% prednisolone acetate or 0.1% dexamethasone every 6 hours. Subconjunctival or intravesical corticosteroid injections may also be given. A potential role for corticosteroids is maintenance treatment after induction of remission with azathioprine.

In more severe cases or in the absence of an obvious response to the initial treatment, azathioprine is prescribed in parallel at an initial dose of 2 mg / kg, then the dose is gradually reduced over 1 to 2 months. Before prescribing azathioprine, a general and biochemical blood test must be obtained. Periodic monitoring of hematological parameters is required, especially during the first months of treatment, due to potential side effects (hepatotoxicity, myelosuppression and gastrointestinal disturbances). The minimum maintenance dose for topical corticosteroids and azathioprine should be determined individually. Relapses are possible, in which drug therapy must be more aggressive before remission occurs.

In addition to lamellar keratectomy, beta irradiation and cryosurgery may be successful in the treatment of EGE. But they are usually not used due to the high effectiveness of drug therapy.

Corneal sequestration

Corneal sequestration occurs only in cats. This violation has a pathognomonic appearance and consists in various pigmentation and necrosis of the stroma. These are brown or black plaques that can be accompanied by vascularization and corneal edema. The sequestrum can be slightly raised above the surface of the cornea, and the overlying epithelium is absent. Corneal sequestration is often caused by herpesvirus infection, but it can also be the result of any persistent irritation, especially entropion. All cats with corneal sequestration should undergo virologic testing for herpesvirus infection.
Treatments for corneal sequestration remain controversial. Because sequesters can peel off spontaneously, conservative monitoring of this disease is sometimes chosen. Affected cats often develop soreness, epiphora, and blepharospasm, so keratectomy is recommended to ensure that healing is fast enough. For cats with positive herpesvirus test results, concomitant antiviral therapy is indicated.

Eosinophilic keratitis

Eosinophilic kereatitis is a feline disease characterized by proliferative white or pink vascularized edematous lesions in the medial or lateral limbus of one or both eyes. The diagnosis is made on the basis of finding eosinophils in biopsies. The pathogenesis of eosinophilic keratitis is not fully understood, but most of the affected corneas were positive for herpesvirus.
Eosinophilic keratitis usually responds well to drug treatment, but relapses can occur if supportive treatment is not taken. Medical treatment consists of topical corticosteroids or systemic megestrol acetate (Ovaban, Schering-PlowAnimalHealth). To control violations, a 0.1% dexamethasone suspension or a 1% prednisolone acetate suspension can be instilled every 6 hours. However, corticosteroids can exacerbate herpesvirus infection, so cats that are positive for herpesvirus are given concomitantly antiviral drugs - for example, trifluridine (Viroptic, BurroughWellcomeCo).

On the other hand, sick cats are given megestrol acetate 5 mg daily for 5 days, reduced to 5 mg every other day for 7 days, and then 5 mg weekly as maintenance treatment. The disease usually responds very well to this treatment. The disadvantage of megestrol acetate is its possible side effects - the development of pyometra and diabetes mellitus, but these are rare.

Florida Spots

Florida spots (acid resistant keratopathy) are corneal lesions that can occur in dogs and cats living in tropical and subtropical climates. These are multifocal, grayish, non-ulcer round lesions of the corneal stroma. The density of the violation increases towards the center. The symptoms of inflammation and irritation are mostly absent. Etiology is uncertain, but infection with acid-fasting bacteria is considered the most likely cause. It is a self-limiting disorder and there is no effective treatment for it.