Felipedia

Retinal diseases in cats

©Barnett, KC & Crispin, SM Feline Ophthalmology (2002) Saunders

The fundus of the eye is the posterior part of the globe viewed ophthalmoscopically and includes the appearance of the retina, superimposed over the underlying choroid abd sclera and divided into tapetal and non-tapetal portions, the optic disc (optic nerve head or papilla) and the retinal blood vessels. The feline fundus is more regular and shows less variation than any of the other domestic animals and certainly less than that of the dog.

The retina is usually considered to have ten layers. The outermost layer, the retinal pigment epithelium, which lies next to the choroid, is derived from the outer layer of the optic cup (ectoderm) whereas the remaining nine layers, the neurosensory retina, develop from the inner layer of the optic cup (also ectoderm). The pigment epithelium is pigmented except over the tapetum, as is the case in all animals with a tapetal fundus.

The vascular pattern of the feline retina is classified as holangiotic, as is the case in the dog, with a direct blood supply to most of the retina. There are three major pairs of cilioretinal arterioles and slightly larger, and usually less tortuous, veins which leave at or near the edge of the optic disc, and extend towards the periphery, leaving the central portion of the disc, unlike the dog, free from blood vessels. A central retinal artery is not usually present in this species but has been reported.

The classification of feline retinal diseases differs between authors and is complicated by the fact that many cases may have an unknown etiology, even after detailed investigation. Feline retinal disease is often associated with systemic disease and a full eye examination, in particular the fundus, should always be included as part of the clinical examination of the sick cat and in a significant number of cases may be of considerable aid in diagnosis.

The normal fundus

The cat has a very well developed, highly reflective, cellular tapetum. The shape is triangular, the appearance granular and the colour usually yellow to green, sometimes blue. Incomplete tapetal development with many islets of colour on a pigmented background is rare in the cat, but has been recorded. Absence of the tapetum occurs in some blue-eyed, white, colour-dilute cats, in others the tapetum is thin with visible choroidal vessels similar to that in blue merle dogs. The area centralis, an area of maximum cone density similar to the fovea, is situated approximately 3mm lateral to the optic disc. This region is devoid of blood vessels and is sometimes a darker green colour. This part of the tapetal fundus is of particular importance in taurine deficiency retinopathy or feline central retinal degeneration. Peripapillary rings of pigment or hyper-reflectivity (conus) are often present or may be absent. The nontapetal fundus is usually heavily pigmented and dark grey-brown in colour. In breeds such as the Siamese and Himalayans, which lack ocular pigment, the nontapetal fundus may be described as tigroid with visible choroid vessels due to lack of pigment in the retinal pigment epithelium; choroid pigment may also be lacking in some blue-eyed, white individuals and a few cats have patches of subalbinism in the nontapetal area. The tapetal junction with the nontapetal area is usually clearly defined but occasionally tapetal islets may be present.

Retinal diseases are often diagnosed using an ophthalmoscope, where a light is passed onto the back of the eye, visualising the retina. Pictures below illustrate various diseases and their impact on normal retina appearance.

Figs. 1-5. Normal retinal fundus in cats

Fig. 6-9. Semi-transparent iris (albino cat), advanced retinal disease, progressive retinal atrophy and retinal haemorrhage following trauma

Figs. 10-12. Gross anaemia and two cases of taurine deficiency

Congenital and early onset abnormalities

Retinal dysplasia is usually secondary to viral infections such as panleucopenia and feline leukemia, but also associated with physical and chemical insults. Retinal dysplasia may occur as an isolated finding, or in conjunction with other ocular defects such as cataracts and microphthalmos. Sometimes the cause is not obvious. The teratogenic effects of feline panleucopenia virus are well documented. In addition to causing cerebellar hypoplasia, the virus may damage the developing retina, resulting in large focal or multifocal areas of retinal degeneration. There is no treatment.

Colobomatous defects involving some or all of the optic disc, peripapillary area, choroid and sclera are rare in cats. Visual problems are unlikely and the defects may be discovered incidentally during ophthalmic examination. Occasionally, other congenital defects may be present.

Lysosomal storage diseases such as GM₁- gangliosidosis can cause retinal changes in the form of multiple small spots, which represent the accumulation of glycolipid within the ganglion cells. A dull, grey, granularity of the area centralis has been described in alpha-mannosidosis. In a proportion of cats with mucopolysaccharidosis type IV and the single case of mucolipidosis type II, the appearance was described as diffuse generalised retinal degeneration. All affected animals show neurological signs in the first few months of life.

Acquired retinal diseases

Hyperviscosity

Hyperviscosity may be a consequence of too many circulating red cells (polycythemia) or raised plasma protein levels (hyperproteinemia). Polycythemia may be primary or secondary. Secondary polycythemia may be a consequence of heart disease or various types of pulmonary insufficiency. Congenital heart diseases such as the tetralogy of Fallot (ventricular septal defect, pulmonary stenosis, dextraposed aorta and right ventricular hypertrophy) are associated with secondary polycythemia because of arterial hypoxemia and affected animals will also be cyanotic because of right to left shunting. There are many reasons for hyperproteinemia, including monoclonal gammopathies such as plasma cell myeloma and plasmacytoma and polyclonal gammopathies associated with immune-mediated disorders (e.g. systemic lupus erythematosus) and chronic antigenically stimulating diseases (e.g. feline infectious peritonitis).

The ocular features are striking and characteristically affect the retinal veins which appear engorged (sometimes like a string of sausages) and tortuous. A few retinal haemorrhages may also be present and the optic disc may be oedematous. Effective management of hyperviscosity syndromes depends upon establishing and treating the underlying cause.

Lipaemia retinalis

Lipaemia retinalis is an ocular manifestation of chylomicronemia (excessive quantities of large triglyceride-rich lipoproteins) and it may be seen in association with both primary and secondary hyperlipoproteinemia, or more specifically hypertriglyceridemia . A primary inherited type has been demonstrated to be caused by defective lipoprotein lipase activity as a consequence of mutation in the lipoprotein lipase gene; all affected kittens have fasting lipemia and a high proportion have peripheral neuropathies which are progressive unless a low-fat dietary regime is instituted.

A transient hyperlipoproteinemia associated with anaemia (a packed cell volume <11%) has been reported and in these 4-5 week-old kittens the chylomicronemia occurred at about the time of weaning. While there may be an hereditary element in this type, other factors (fleas, Haemobartonella felis and high fat intake) are involved and provided that the condition is recognised and treated (oxygen-rich atmosphere and whole blood transfusion for the acute anaemia, doxycycline for H. felis infection reduction of flea burden by daily combing and weaning onto a low-fat diet) the condition resolves completely. In older animals, secondary hyperlipoproteinemia associated with raised triglycerides is seen most commonly in association with diabetes mellitus and megestrol acetate administration.

Lipaemia retinalis is most readily observed against the dark background of the nontapetal fundus and lipemia is easier observed if the patient has a low hematocrit as there are fewer red blood cells to obscure the creamy plasma.

Haemorrhage

Retinal haemorrhage is not unusual in the cat and may have a variety of causes. Blunt and penetrating injuries are common causes of retinal and choroidal haemorrhage. Anaemic retinopathy and thiamine deficiency, as a consequence of thiaminase-rich diets or low thiamine content has a variety of effects which include dilated retinal vessels, retinal haemorrhages, neovascularisation and peripapillary , as well as neurological signs, and culminates in coma and death in unrecognised cases. Inflammatory retinopathies may be associated with haemorrhage (e.g FIP) and migrating parasites can produce haemorrhage. Haemorrhage may also be a consequence of primary and secondary neoplasia. Hypertension is one of the most common causes of retinal and choroidal haemorrhage. Hemostatic disorders are not regularly associated with intraocular haemorrhage.

Retinal detachment

Retinal detachment results when the neurosensory retina separates from the underlying retinal pigment epithelium, The causes of retinal detachment include hypertension, inflammation, trauma, neoplasia, hyperviscosity syndromes and ethylene glycol poisoning. The pathogenesis of retinal detachment depends upon the cause; hypertensive changes, inflammatory choroidal and/or retinal exudates can result in bullous and exudative detachment; trauma-induced and post-surgical holes and tears can produce rhegmatogenous detachments; neoplasia can infiltrate the choroid and/or retina to produce a solid detachment. Traction detachments as a result of the formation of post-inflammatory vitreal traction bands are not usually recognised in cats.

Management of retinal detachment depends upon establishing the cause. Unfortunately, degeneration of the feline retina begins within 1 hr of detachment and the changes are progressive and usually irreversible, so prompt treatment to initiate retinal reattachment is critical for retinal regeneration.

Hypertension

Sudden onset blindness associated with retinal detachment and/or intraocular haemorrhage is the most perceptible indicator of the presence of systemic hypertension. Unfortunately, advanced, irreversible pathology underlies these ocular manifestations and it must be stated unequivocally that the successful management of hypertension in cats depends upon early recognition, accurate diagnosis and effective, well-monitored treatment. The problem is most commonly recognised in older cats (average 14-15 yrs) although regular health checks of older cats indicate that early hypertensive changes may be detected at a younger age (average 11-12 yrs). It is important, however, to emphasise that hypertension can be a clinical problem in younger animals.

Hypertension is a common feline problem; it may be primary or secondary. Secondary causes of feline hypertension include renal disease, thyroid disease ( hyperthyroidism), chronic anaemia, diabetes mellitus, megestrol acetate administration, chronic corticosteroid usage (iatrogenic hyperadrenocorticism) and primary aldosteronism. Detailed laboratory investigation is therefore essential and the situation is further complicated because established hypertension will cause other organs to dysfunction (e.g. glomerulosclerosis, left ventricular hypertrophy, hypertensive encephalopathy).

The eye appears to be particularly susceptible to the effects of hypertension and it is fortunate that it is so accessible to detailed examination. The earliest changes of hypertension which are likely to be observed probably originate from choroidal vessels and consist of focal, slightly hazy, opacities overlying the choriocapillaris which are easiest to observe against a tapetal background; these might reflect incompetence of the choriocapillaris with leakage of plasma and fibrinogen. It may be that choroidal vessels are affected earlier and more severely than retinal vessels because of their anatomical arrangement and because they lack the autoregulatory control of blood flow found in retinal vessels. If hypertension persists there will be further damage to choroidal vessels and small, focal intra-retinal haemorrhages may be observed.

Retinal detachment is a likely consequence of ischaemic damage to the retinal pigment epithelium and sub-retinal exudation. Diurnal fluctuations of blood pressure probably account for the variations of appearance (flat detachments, reattachment with retinal folds) which may be seen in many early cases on sequential examination. Flat detachments typically accompany the early changes detectable ophthalmoscopically, but more extensive bullous retinal detachment (usually multiple bullae), perhaps even total detachment, will follow if blood pressure remains high.

Hypertensive retinopathy in older cats

Older cats can present with sudden blindness due to serous retinal detachments secondary to systemic hypertension. Treatment is with the calcium channel blocker Amlodipine (Norvasc - 0.625 mg/cat) and systemic corticosteroids (prednisone, 0.5-1 mg/kg, PO) to help control the posterior inflammation. Retinas can re-attach once blood pressure returns to the normal range. At least 50% of cats regain some clinical vision if treated early.