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Acquired Diseases of the Retina and the Choroids
A. Regnier
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The canine and feline acquired retinal and choroidal diseases can be subdivided by etiology into inflammatory, vascular, metabolic, nutritional, iatrogenic, and miscellaneous.
I- Inflammation of the Choroid and Retina
Due to the choroid and retina apposition, the latter is often involved with choroidal inflammation. Because it is difficult to distinguish retinitis from choroiditis, the term chorioretinitis is used. The inflammation of the retina/choroid may result from either a traumatic, infectious, or immune mediated process. Visual effects depend on the degree of involvement. Often chorioretinitis is observed while performing ophthalmoscopy as part of a general examination or is diagnosed when blindness results. The ophthalmoscopic appearance of chorioretinitis varies with the nature, extent, location and duration of inflammation. In contrast to the inherited retinopathies, chorioretinitis lesions are seldom symmetrical and initially may be only unilateral. As concurrent anterior and posterior uveal inflammation is possible, the posterior inflammation may be difficult to visualize if the involvement of the anterior segment is severe. Acute or active inflammatory changes present initially as multifocal areas of retinal oedema with or without perivascular changes. They appear as grey lesions, circular or with indistinct edge. A haze may be present in the area adjacent to the lesion or throughout the vitreous. Retinal or subretinal haemorrhages may also be present. Accumulation of subretinal exsudate or granuloma may result in retinal elevation or detachment. As a general rule, infectious diseases result in more perivascular and subretinal exudate than the traumatic, or immune-mediated diseases. In severe cases, subretinal exudate may lead rapidly to a total retinal detachment. As the inflammation subsides, chronic or inactive changes may appear as sharply demarcated areas of tapetal reflectivity or clumps of pigmentation surrounded by areas of increased reflectivity. In the nontapetal region, sharp depigmented areas with or without pigment clumping are typical of scars.
In dogs, various infectious diseases have been documented to cause chorioretinitis, including canine distemper, brucellosis, ehrlichiosis, leptospirosis, toxoplasmosis, systemic mycosis, and bacterial septicaemia. Concurrent active infections with canine distemper virus and toxoplasmosis have, for uncertain reasons, been recorded. Ocular involvement is common in dogs with leishmaniasis. Blepharitis, keratoconjunctivitis and uveitis are the most common signs. The posterior segment may be involved by extension from the anterior parts of the eye. In cats, chorioretinitis can be caused by toxoplasmosis, feline infectious peritonitis (FIP), Bartonella and systemic mycosis. Chronic anterior uveitis is seen in association with FIV infection but its exact role remains undetermined. The presence of a pars planitis indicates the possible involvement of the posterior segment. Parasitic granulomatous chorioretinitis has been associated with intraocular larval migration of Toxocara canis in dogs, and curvilinear tracts in the ocular fundus secondary to ophthalmomyasis interna have been reported in dogs and cats
Immune-mediated diseases that can be associated with chorioretinal lesions include the uveodermatologic syndrome in dogs and periarteritis nodosa in cats.
Attempts to diagnose the cause of chorioretinal lesions are usually limited to animals with active lesions. The fundic lesions are rarely distinctive enough to identify the cause. Because active chorioretinal changes may occur along with other signs of a systemic disease, the diagnostic approach should include a detailed history, complete physical examination, and specific laboratory tests. Vitreous paracentesis is a helpful diagnostic test with systemic mycoses.
Treatment of chorioretinitis is attempted only in the acute cases and often is determined by the concurrent systemic state. Although systemic corticosteroid therapy is usually warranted, these drugs are contraindicated in cases of chorioretinitis associated with infectious disease processes.
II- Acquired Retinal Degenerations
A- Sudden Acquired Retinal Degeneration (SARD)
This condition has also been called metabolic toxic retinopathy or silent retina syndrome. These dogs are presented with a history of acute blindness. Affected individuals are middle age to old (exact age may vary with breed type) and vision loss is often accompanied by polyuria/polydipsia, polyphagia, and a recent history of weight gain. Any breed can be affected, but the dachshund and Brittany spaniel breeds are at elevated risk.
On ocular examination, the pupillary light reflexes may be very sluggish or totally absent. Initially, lesions in the posterior segment may be totally absent, but over subsequent weeks and months, fundic lesions develop which are typical of retinal atrophy. These changes include tapetal hyperreflectivity and attenuation of retinal vessels. Unlike inherited progressive retinal atrophy, lesions in the nontapetal area do not include pigment changes, such as depigmentation.
Initial diagnosis is based on the history, age, physical appearance of the dog, and the lack of significant fundic lesions. Confirmation is based on the slow progression of ophthalmoscopic signs and undetectable electroretinographic responses to white light stimulation.
The cause of SARD is not clearly defined. Laboratory abnormalities consistent with hyperadrenocorticism are common although definitive biochemical proof of the disease is often lacking in dogs with SARD. However, most affected dogs have elevations in sex hormones indicating increased adrenal activity. The presence of autoantibodies directed against retinal proteins has not been identified in SARD-affected dogs. Histologically, retinal inflammation is minimal, and apoptosis appears to be the mechanism of photoreceptor cell death in affected animals.
B- Nutritional Retinal Degenerations
Taurine deficiency retinopathy is well known in cats. Taurine is poorly synthesized from cysteine or methionine in the feline species and as such it is an essential nutritional requirement. Deprivation either as a result of poor uptake from an adequate dietary source or as a straight dietary deficiency produces retinal degeneration and dilated cardiomyopathy which may not be present at the same time in an affected cat. As taurine functions as a neurotransmitter in the retina and is possibly necessary in maintaining the structural integrity of the photoreceptor membrane, retinal lesions result from photoreceptor degeneration. The initial retinal lesions appear as an increase in granularity in the area centralis, to enlarge and become oval hyperreflective areas. Then, a second hyperreflective area medial to the optic disc is seen in the following stage of the disease. Generalized retinal degeneration with diffuse hyperreflectivity and vascular attenuation eventually occurs. Taurine intake (110 mg/kg BW) will arrest the central retinal degeneration, but will not restore sight in patients with advanced retinal degeneration.
Nutritional deficiency of vitamin E in dogs can lead to pathological changes of the retina that are essentially the same as those of the retinal pigment epithelial dystrophy, formerly known as central progressive retinal atrophy, which has been described in several breeds of dogs. vitamin E-deficient dogs are usually examined because of progressive vision loss. Fundic lesions include tapetal hyperreflectivity, vascular attenuation and multifocal brown pigment clumps from lipofuscin accumulation. Affected dogs can also show clinical signs of neurological dysfunction including ataxia, proprioceptive deficits, abnormal spinal reflexes and muscle weakness. vitamin E supplementation can stabilize the neurological signs but does not improve dogs’ vision.
C- Drug-induced Retinal Degenerations
The association between enrofloxacin administration and the acute onset of retinal degeneration has been reported in the cat. Results of clinical studies indicate that the enrofloxacin-induced retinal degeneration in cats is rare and idiosyncratic.
Histopathologically, it has been shown that the drug may be toxic to the rod photoreceptors leading to atrophy of the outer retina. The cats’ age, sex, and medical condition seem unrelated to the drug toxicity.
Retinal degeneration secondary to ivermectin toxicity is uncommon in the dog, and results from incidental ingestion of ivermectin based equine or bovine dewormer a few hours prior to onset of an acute vision loss. These individuals may or may not have a history of seizuring at the time of onset of blindness. Visual loss is usually reversible.
III- Retinal Vascular Disease
A- Hypertensive Retinopathy
Systemic hypertension is seen in both dogs and cats, but the highest incidence is in the geriatric cat. Hypertension can cause tortuosity of retinal vasculature, retinal oedema and hemorrhage, vitreal hemorrhage, occasional hyphema and varying degrees of retinal detachment. Most cases with retinal detachment are presented to the ophthalmologist due to acute blindness in one or both eyes. If a severe vitreal hemorrhage precludes examination of the fundus, B-scan ultrasonography of the globe is usefull to identify the retinal detachment. Primary or essential hypertension is rare, and is diagnosed on the basis of the exclusion of all other potential causes. Secondary hypertension will occur with renal disease, hyperthyroidism, hyperlipidemia, pheochromocytoma, Cushing’s syndrome, or diabetes mellitus. Renal disease and hyperthyroidism are the two most common etiologies in cats.
At the time of presentation, the prognosis for sight in the severely affected patients is poor but some control of the hypertension can be attempted. The definitive diagnosis of systemic hypertension in dogs and cats is based on indirect measurement of blood pressure. The reliability of the values is dependent on proper technique and equipment including the right size cuff. Systolic pressures greater than normal with compatible lesions are considered diagnostic by most authors.
Treatment of hypertension must first be directed at the primary etiology. Depending on the etiology, therapy may consist of one or more of the following: low salt diet combined with diuretics, beta-blockers, angiotension-convertingenzyme inhibitors, calcium channel blockers, or/and valodilators. Systemic prednisolone has been used in cases of severe retinal involvement. If not contraindicated by pre-existing disease, the anti-inflammatory action helps reduce the retinal oedema and subretinal transudate associated with the retinal detachment. Improvement of vision and ocular signs may be seen following control of the hypertension but may take up to six to eight weeks. Some patients may regain vision despite the fact the hypertension is not fully controlled. Some cats may not regain vision due to severe retinal involvement that results in total atrophy.
B- Diabetic Retinopathy
Diabetic retinopathy occurs in dogs, but the retinal changes are less extensive and severe than the retinal lesions in the human counterpart. The cataract formation is an early finding in the disease of dogs and often the reason for a patient with diabetes to be presented for the first time. In man the vascular changes in the retina are of major importance in the disease and contribute to blindness. By contrast, in spontaneous canine diabetes mellitus the anomalies of the retinal vasculature are less severe and of minor clinical importance.
It is known from experimental models in dogs that the initial retinal vascular changes is the formation of micoraneurysms, resulting from the sacculation of a small area of the capillary wall. Rupture of these aneurysms results in ophthalmoscopically visible focal hemorrhages, and there may be accompanying exudation. In a recent study it was found that 21% of diabetic dogs developed ophthalmoscopic signs of diabetic retinopathy, and the medium time from diabetes diagnosis to appearance of retinopathy was 1.4 years. In man, proliferative changes may also develop, which include preretinal and vitreal neovascularisation, often with connective tissue formation in the vitreous.
C- Retinal Haemorrhages
Haemorrhages are common manifestations of severe anemia with hemobartonellosis, feline leukemia complex, and thrombocytopenia. When the hematocrit falls to 10 - 12% haemorrhages are common and not dependent on a thrombocytopenia. They can be located preretinal (bright red and large), nerve fiber layer (flat striated) or intraretinal (punctuate red dots). Correction of the anemia results in rapid resolution of the smaller lesions, although permanent pigmentary changes may be noted. Systemic hypertension, hyperviscosity syndromes, diabetes mellitus, thiamine deficiency, and ocular trauma may also induce retinal haemorrhages. Systemic hypertension should be considered the primary differential in all geriatric cats with intra-ocular haemorrhage. Retinal detachment can be associated with retinal haemorrhages in case of systemic hypertension, hyperviscosity syndromes, and ocular trauma.
IV- Retinal Detachments
Retinal detachment (RD, retinal separation) is an important cause of vision loss in dogs and cats. Separation of the sensory retina from the underlying pigmented epithelium may occur secondary to a tear in the sensory retina (rhegmatogenous RD), traction on the retina from the vitreous humour (traction RD), or fluid or cell accumulation in the subretinal space (exsudative RD).
Ophthalmoscopically, areas of RD appear as focal greyish areas within the tapetal and non-tapetal fundus. A more extensive RD is recognized by a pale grey transparent veil containing the retinal vessels and protruding into or waving in the vitreous. As such it will no longer be observed within the normal plane of the retina. When retinal dialysis is present and the dorsal retina has fallen into the ventral part of the vitreous cavity, hyperreflectivity of the dorsal tapetal region with no retinal blood vessels may be noted.
Exsudative or serous retinal detachments occur as a result of a chorioretinitis, retinal vascular disease secondary to systemic hypertension, ocular trauma, ocular neoplasia or idiopathic process. Idiopathic serous retinal detachments have been reported in dogs less than one year of age and appear to occur more commonly in German Shepherds than in other breeds. Affected dogs are presented with a history of acute blindness; mild conjunctival hyperaemia and aqueous flare are normally present. The pupillary light reflexes, if present, are sluggish. On ophthalmoscopic examination, the retina may be totally elevated due to large amounts of subretinal fluid. The subretinal fluid may gave a pink-gray discoloration, but retinal haemorrhage is seldom seen. Initial treatment consists of oral prednisolone at an immunosuppressive dose. Aggressive therapy will continue until the entire retinal is flat and free of edema. With improvement, the oral prednisolone is reduced to alternate or every third day. Vision often will return regardless of the subsequent development of ophthalmoscopic signs of multifocal retinal degeneration.
Traction RD occurs when contraction of vitreous bands allows the sensory retina to move forward from its position against the choroid. This occurs as the result of inflammatory and/or fibrotic tissue bands developing within the vitreous body. Thus, traction RDs may be secondary to ocular trauma, intraocular haemorrhage or posterior segment inflammation. This type of RD is rarely amenable to medical or surgical treatment in dogs and cats.
Rhegmatogenous RDs result from holes or tears in the sensory retina, which allow liquefied vitreous to enter the subretinal space. This process has been reported in old dogs, in dogs with hypermature cataract, lens luxation, and may represent a complication of intraocular surgery. Surgical treatment of rhegmatogenous DR is possible but is rarely undertaken in small animals.
V- Retinal and Choroidal Tumors
Canine lymphosarcoma has been associated with posterior segment involvement resulting in retinal haemorrhage and detachments. Metastatic hemangiosarcomas and metastatic adenocarcinomas can result in retinal haemorrhage and detachment in the dog and cat. The feline leukaemia complex and leukemias may produce fundus lesions which vary considerably in appearance. They include multifocal gray infiltrates, diffuse mottling of the tapetum, bullous retinal detachment, and perivascular infiltration. Definitive diagnosis is usually based on concurrent systemic signs and tests. Regression may occur with cancer chemotherapy.
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1. Van der Woerdt A, Nasisse MP, Davidson MG. Sudden acquired retinal degeneration in the dog: clinical and laboratory findings in 36 cases. Prog Vet Comp Ophthalmol 1991;1:11-18.
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