Clinicians should recall that the posterior segment of the eye provides a direct look at blood vessels and the central nervous system and can offer valuable information in patients suspected of systemic infectious disease, neoplasia, vascular disorders, hypertension or central nervous system (CNS) disease. Do not reserve evaluation of the posterior segment for only those patients with altered vision.
Acquired fundus abnormalities related to systemic infection, neoplasia, hypertension, nutritional deficiency or drug toxicity are more likely to be encountered in the cat than congenital or inherited disorders.
Chorioretinitis and optic neuritis are terms used to describe inflammation of the posterior segment. Unless vision is affected or other ocular tissues are concurrently inflamed, the eye may appear unremarkable until ophthalmoscopy is performed. Active inflammatory lesions in the tapetal fundus appear as poorly defined areas of decreased reflectivity due to accumulations of cells and/or oedema within the retina, between the neural retina and retinal pigmented epithelium (RPE), or within the choroid. Similar lesions in the non-tapetal region are likely to appear grey or white in colour as the infiltrates obscure underlying pigment. Focal thickening of the retina may appear in folds. Retinal blood vessels may be elevated or obscured by infiltrates. Cellular infiltrates along retinal vessels (perivascular cuffing) are more easily seen in the non-tapetal fundus. Haemorrhages may occur, such as those attributed to pancytopenia in feline leukaemia virus (FeLV)-positive patients. Sufficient subretinal exudates or transudates will cause retinal elevation and detachment.
The presence of chorioretinitis and/or optic neuritis is suggestive of systemic disease until proven otherwise. Causes of chorioretinitis in cats are also likely to produce concurrent anterior uveitis. Physical and laboratory examinations are indicated to rule out various infectious and neoplastic aetiologies. Figure 1 lists diseases that have been associated with feline chorioretinitis. The most likely causes of optic neuritis include feline infectious peritonitis, cryptococcosis, toxoplasmosis and lymphosarcoma.
To treat chorioretinitis or optic neuritis effectively, the underlying cause must be targeted. Otherwise, antiinflammatory or immunosuppressive doses of systemic corticosteroid are indicated to preserve retinal and optic nerve function. Prognosis for vision is guarded in patients with secondary retinal detachment or optic neuritis, regardless of cause.
Figure 1. Diseases associated with feline chorioretinitis.
Feline infectious peritonitis
Feline leukaemia virus
Feline immunodeficiency virus
Feline herpesvirus-1 (?)
Orbital inflammatory disease
Retinal detachment refers to separation of the sensory retina from the underlying RPE. Total detachment may be observed with a penlight as a white to grey veil 'floating' behind the lens. Less extensive detachments appear ophthalmoscopically as defocused areas that obscure underlying detail and alter the course of nearby retinal vasculature. Unilateral detachments may go undetected but obvious vision impairment occurs with bilateral involvement. The pupils are typically dilated when both retinas are completely detached, although pupillary light responses may persist for some time. Remember that the presence of a pupil response does not equate with vision.
While a variety of aetiologies such as trauma and inflammation can lead to retinal detachment, systemic hypertension is the most common cause of retinal detachment in the geriatric cat. Fundus changes are a consequence of tissue ischaemia, with effusion and haemorrhage secondary to alterations in vascular integrity. Routine funduscopic examination in older cats may identify early evidence of hypertension, including foci of retinal oedema, small intraretinal 'dot' or 'flame' haemorrhages and/or increased prominence or tortuosity of retinal blood vessels. Widespread retinal detachment and haemorrhage within the retina or vitreous are usually associated with more dramatic elevations in blood pressure. These cats typically present with sudden loss of vision. On rare occasions, hyphaema is seen. Those patients with extensive subretinal and vitreous haemorrhage have a poorer visual prognosis.
Diagnosis is based on signalment, clinical signs and documentation of blood pressure elevations (systolic pressure above 180 mmHg or diastolic pressure above 95 mmHg). Hypertensive cats should be evaluated for chronic renal failure, hyperthyroidism, diabetes mellitus and cardiac abnormalities. Amlodipine besylate is the antihypertensive of choice in the cat. An initial oral dose of 0.625 mg q24h is safe and often effective, particularly when initiated soon after vision loss occurs. Researchers have advocated doses as high as 1.25 mg q12h in cats with severe hypertension. Recent dosage recommendations for amlodipine expressed in mg/kg (0.18 mg/kg ± 0.03 mg/kg q 24h orally) may provide for better individual tailoring of the dose. An estimated 70% of cats experience improvement in ocular signs, including return of vision, in response to amlodipine. The more chronic the detachment, the less likely that vision will return, even though the retina may reattach. Post-detachment retinal degeneration is characterised by retinal vessel attenuation and tapetal hyperreflectivity.
Acquired Retinal Degenerations
Enrofloxacin-Associated Retinal Degeneration
Acute retinal degeneration is sporadically seen with enrofloxacin administration in cats. No age, breed, or sex predilection has been determined, but older cats appear to be over-represented in reported cases. The toxicity is most commonly seen with doses above the manufacturer's recommendation of 5 mg/kg once a day, or with routes of administration other than that approved by the manufacturer. In a published retrospective series, one cat received <5 mg/kg once daily for 8 days prior to the onset of clinical signs. Clinical signs include an acute onset of mydriasis and decrease in vision; blindness is common. Owners have noted changes in pupil size after only two doses of the drug.
During the acute stage of the toxicity, the retina appears normal. Electroretinographic examination reveals a lack of recordable response, suggesting diffuse extensive outer retinal disease. Subsequent posterior segment changes include tapetal hyperreflectivity and retinal vascular attenuation, typical of retinal degeneration but notable for the rapidity with which they occur. Return of vision is possible after prompt discontinuation of the drug in acutely affected patients, but blindness is often irreversible in more chronic cases.
Feline Central Retinal Degeneration
Feline central retinal degeneration (FCRD) is caused by a nutritional deficiency of taurine, a disorder unique to cats. At present, all US commercial cat foods contain an adequate concentration of taurine for the vast majority of cats, making this disease rare among cats that are fed a proper diet. It is still sporadically seen in cats that are fed either homemade diets or dog food. In addition, it is occasionally seen in cats on an appropriate diet, suggesting that the requirement for taurine may be even higher for selected cats.
Taurine deficiency affects first the cone photoreceptors most prominent in the area centralis dorsotemporal to the optic disc. Deficiency results in bilaterally symmetrical elliptical areas of hyperreflectivity that appear first in the area centralis. As the disease progresses, similar lesions appear dorsomedial to the optic disc. Gradually, the two lesions converge creating a hyperreflective band dorsal to the optic nerve. If left untreated, slow progression throughout the entire retina may result in blindness. Correction of the taurine deficiency will stop progression of the disease, but will not result in correction of lesions that are already there. Affected cats should be monitored for cardiomyopathy.
Vascular and Haematological Disorders
Retinal vessel congestion and dramatic vascular tortuosity occur in cats with polycythaemia secondary to congenital cardiovascular anomalies. Transudative retinal detachment may develop, perhaps secondary to hyperviscosity. Similar vascular changes may occur as a consequence of lymphosarcoma-associated hyperviscosity. Severe anaemia with PCVs less than 7% manifest as pale retinal vessels and varying degrees of retinal haemorrhage, irrespective of the platelet count. Not surprisingly, the haemorrhage is more extensive when the anaemia is combined with thrombocytopenia. Haemorrhage associated with neoplasia is probably secondary to vasculitis rather than platelet deficiency.
Lipaemia retinalis is characterised by a pinkish rather than dark red retinal vessel colour as serum triglycerides elevate above 2500 mg/100 ml. It is easier to visualise the vascular colour change over the non-tapetal region. Elevations in serum cholesterol are not as likely to affect the retinal vasculature.