Ординатура / Офтальмология / Английские материалы / Notes on Veterinary Ophthalmology_Crispin_2005

FELINE OPHTHALMOLOGY

VITREOUS

Congenital disease of the feline vitreous is very rare, and acquired problems, as in other species, are usually a consequence of extension from neighbouring structures (e.g. snowflake opacities in pars planitis; intravitreal haemorrhage because of bleeding from retinal vessels in systemic hypertensive disease).

OCULAR FUNDUS

ANATOMY

The feline globe is well adapted to vision under dim lighting conditions (relatively large eye, large diameter cornea, large lens, rod-dominated retina and a highly efficient tapetum). Because the tapetum is highly reflective and the normal pupil constricts readily to a vertical slit, fundus examination should be performed with very low levels of illumination.

The fundus shows fewer variations of appearance than the normal canine fundus (Figures 4.1(b), 4.39(a,b) and 4.40(a,b)). The optic disc or optic nerve head (ONH) is circular and is located in the tapetal fundus when a tapetum is present. The retinal vessels often hook over the edge. It is not unusual to see a rim of pigment or other colour surrounding the disc: the latter variant may appear reflective and is known as conus.

observed in the retinal nerve-fibre layer. The physiological pit is often obvious and the ONH appears slightly ‘cupped’ in most cats, a detail more readily appreciated using the slit beam option on a direct ophthalmoscope.

Different fundus appearances are largely related to the amount of pigment present and the presence or absence of a tapetum. The tapetum develops postnatally and its colour varies between yellow to green, sometimes blue. Sub-albinotic eyes are usually atapetal (Figure 4.40(a)).

The retinal blood supply is holangiotic. The usual pattern of retinal vessels consists of three major cilioretinal arterioles and a similar pattern of veins, the veins being of greater diameter and slightly darker than the arterioles. In the commonest fundus appearance, choroidal vessels, which perforate the tapetum to supply the choriocapillaris, may be viewed end on against the tapetal background. In colour-dilute cats where the fundus lacks pigment, or those in which there is no tapetum, considerably greater detail of the choroidal vasculature is apparent (Figure 4.40(b)).

The area centralis (equivalent of human macula) is located dorsolateral to the optic disc and is usually obvious because of the lack of blood vessels in the region. The area centralis contains the highest concentration of cones in the retina; even so, the feline fundus is rod dominated.

(a)

(b)

Figure 4.40(a,b) Normal sub-albinotic iris (a) and fundus (b) in a blue-eyed Domestic Shorthair.

CONDITIONS OF THE OCULAR FUNDUS

Neurometabolic diseases (lysosomal storage disorders)

•Although the enzyme defect is present from birth in these unusual lysosomal storage disorders, the progressive clinical signs appear later because of the accumulation of substrate in many cells throughout the body. In the retina, retinal ganglion cells and the retinal pigment epithelium are involved. There are more reports of ocular involvement with lysosomal storage diseases in cats than dogs.

•Retinal involvement has been reported in GM1-gangliosidosis, a-mannosidosis, mucopolysaccharidosis (type VI) and mucolipidosis (type II).

FELINE OPHTHALMOLOGY

FELINE OPHTHALMOLOGY

•It is often difficult or impossible to identify the subtle fundus changes (e.g. multiple focal spots) because of accumulation of substrate in the corneal cells, which produces corneal cloudiness.

Retinal dysplasia

•Uncommon in cats and usually associated with perinatal viral infection (e.g. natural infection with feline panleucopenia virus and experimental infection with feline leukaemia virus)

•In addition to impaired retinal development, the development of cerebral and cerebellar tissues may also be affected and the commonest neurological signs relate to cerebellar hypoplasia with feline panleucopaemia virus infection

Inherited progressive retinal atrophy (PRA)

•An autosomal-dominant rod–cone dysplasia observable ophthalmoscopically at 8–12 weeks of age exists in a closed colony of Abyssinian cats at the Animal Health Trust in the UK. There is also an autosomal recessive type of rod-cone degeneration observable ophthalmoscopically at 1.5–2 years in this breed

•The British Shorthair and Siamese are other breeds in which inherited PRA might occur

•The ophthalmoscopic signs of inherited PRA are a bilateral increase in tapetal reflectivity, vascular attenuation and a poor PLR; the changes are symmetrical

•PRA is much less common in cats than dogs and, as in dogs, there is no treatment

Nutritional retinopathies

Taurine deficiency retinopathy

Taurine deficiency produces a retinal degeneration that is most obvious in the area centralis in the early stages, hence the description of feline central retinal degeneration (Figure 4.41). Progression of the condition results in a band-shaped lesion dorsal to the optic disc and eventually there is generalised retinal degeneration and irreversible blindness.

this condition in some cats by feeding unusual diets, for example, exclusively dog food, which lacks taurine. This is because taurine is an essential amino acid for cats, whereas dogs can synthesise their own.

Treatment involves taurine supplementation (the daily requirement for an adult cat is 10mg/kg body weight).

Thiamine deficiency retinopathy

•Thiamine deficiency is unusual and may be a consequence of feeding diets deficient in thiamine (e.g. heat-processed commercial cat foods) or containing thiaminases (e.g. raw fish)

•Clinical signs include anorexia and neurological signs (mydriasis with normal vision, ataxia, ventroflexion of the head and neck)

•Fundus examination may reveal retinal haemorrhage, papilloedema, peripapillary oedema and neovascularisation

•Coma and death result if the condition remains untreated

•Treatment involves thiamine (50–75mg per dose every eight hours) to reverse the deficit, and corticosteroids to reduce the oedema; both may be given intravenously

Infections

Viral infection

Feline infectious peritonitis (FIP)

Fundus changes are associated with vasculitis, pyogranulomatous inflammation or hyperviscosity because of increased protein levels.

Feline leukaemia–lymphoma complex (FeLLC)

Fundus changes are usually a consequence of neoplastic involvement ± anaemia and thrombocytopaenia.

Feline immunodeficiency virus (FIV)

Fundus changes are probably related to concurrent toxoplasmosis.

Bacterial infection

Mycobacteria

Mycobacterial infections may be associated with chorioretinitis and retinal detachment.

Sepsis

Sepsis can produce multifocal inflammatory lesions by haematogenous spread.

Parasitic infection

Toxoplasmosis

The parasite may invade the retina and choroid, but the inflammation it produces is not distinctive and concurrent infection (e.g. FIV) is possible.

Ophthalmomyiasis interna

Dipteran larvae may gain access to the eye and produce highly-characteristic crisscrossing tracks in the fundus.

FELINE OPHTHALMOLOGY

FELINE OPHTHALMOLOGY

Systemic mycotic infection

Fundus changes are usually the result of haematogenous spread and consist of subretinal and intraretinal pyogranulomas.

Neoplastia

•Primary tumours include astrocytoma and meningioma

•Metastatic tumours include lymphoma, squamous cell carcinoma, adenocarcinoma and haemangiosarcoma

•Ophthalmoscopic findings include neoplastic infiltration, retinal detachment, retinal haemorrhage and retinal degeneration

•Ischaemic degenerative changes, including pigmentary disturbance, have been associated with angioinvasive tumours such as primary bronchogenic carcinoma

Trauma

Blunt trauma

•Retinal detachment may be associated with blunt trauma. Although the retina may reattach spontaneously, degenerative changes will mark the site of the original detachment

•Intraocular haemorrhage, including hyphaema, may also be associated with trauma

Penetrating trauma

•Intraocular haemorrhage is the commonest complication

•Prognosis depends upon the site and extent of the injury

•Damage to the lens ± uveal tract may be complicated by malignant intraocular sarcoma formation, sometimes years after the initial injury

Toxic changes

•Acute retinal degeneration/necrosis may follow the administration of substances toxic to the feline retina

•Parenteral enrofloxacin (and possibly other quinolone antibiotics) has been associated with an apparently idiosyncratic adverse reaction. Affected cats become acutely blind, with widely-dilated non-responsive pupils, often within hours of treatment (Figures 2.24 and 4.42)

•Bilateral diffuse retinal degeneration is apparent within a few days of drug administration

•The outer retina, particularly the photoreceptor layer, is damaged

•There is no specific treatment, but there may be a degree of recovery if the association is recognised and the drug stopped immediately

•If this antibiotic is selected for use in cats the dose rate should not exceed 5mg/kg every 24 hours

Figure 4.42 Enrofloxacin-associated retinal degeneration in a Domestic Shorthair. The cat went acutely blind overnight (Figure 2.24, Section 2, p. 58) and bilateral retinal degeneration was apparent within a week of the cat receiving the drug.

Systemic hyper tensive disease

Both primary and secondary systemic hypertension occurs in cats and is certainly the commonest reason for fundus abnormality in older cats. The eye is a sensitive and readily-examined target organ, and ophthalmoscopic examination of both eyes must be performed in any adult cat that presents with haemorrhage in the anterior chamber.

Hypertensive fundus changes and their progression (Figures 4.43–4.45)

•The hypertension-induced damage to the choroidal, retinal and optic nerve head vasculature (mainly the result of ischaemia followed by degeneration) allows serum and even whole blood to escape

•Leakage may first be apparent as focal, hazy areas associated with choroidal vessels, mainly arterioles, which are viewed end on as the ‘stars of Winslow’. These vessels are most easily viewed in the tapetal fundus as they pierce the tapetum en route to the choriocapillaris

•The histology of the normal tapetal retina and choroid is illustrated at the head of this section, and a choroidal vessel perforating the tapetum can clearly be seen (Figure 4.1(a))

•Leakage at this site allows subretinal fluid to accumulate. Subretinal fluid accumulation results in focal bullous retinal detachment

•In the early stages partial retinal detachment may be followed by reattachment in some patients, producing pathognomonic, often localised, branching linear folds, but eventually total detachment will occur if the condition is not recognised

•The retinal vessels become grossly abnormal (variable diameter, notably narrow segments ± aneurysmal dilatations)

•Arterioles are most severely affected

•Haemorrhage from choroidal and retinal vessels can produce marked intraocular haemorrhage and, in some cases, there will also be haemorrhage from iris vessels and hyphaema

•The optic nerve head may become oedematous (papilloedema)

•Retinal detachment and intraocular haemorrhage are the complicating factors most likely to be encountered

•End-stage fundus changes comprise panretinal degeneration and optic atrophy, and,

FELINE OPHTHALMOLOGY

FELINE OPHTHALMOLOGY

although such animals are irreversibly blind, they can still have a good quality of life if the systemic hypertension is treated

• The differential diagnosis of feline panretinal degeneration is summarised later

Diagnosis

It is important to recognise systemic hypertension as early as possible, ideally when the choroidal vessels appear ‘fuzzy’ and there is early mild subretinal fluid accumulation. Vision will be severely compromised or lost once retinal detachment has occurred, as retinal degeneration starts within hours of detachment in the cat. All cats of eight years of age and older should undergo regular screening (including examination of the ocular fundus and blood-pressure measurement) to detect early systemic hypertensive changes.

•History (e.g. to identify secondary associations such as renal failure and hyperthyroidism) and clinical signs

•Systemic arterial blood pressure (if there are no facilities for accurate measurement such as Döppler flow oscillometry, then the cat should be referred)

•Relevant laboratory tests

Management

•Emergency treatment of systemic hypertensive crises may include titrated dosage of sodium nitroprusside and can only be attempted when specialist facilities for continuous monitoring of blood pressure are available. This is unlikely to be available in all but a limited number of referral centres.

•The cause of the systemic hypertension must be investigated to establish whether it is primary or secondary to other conditions such as chronic renal failure or hyperthyroidism.

•Patients can be given good quality of life on medical treatment (usually a low-sodium diet and oral medication). The drugs used most commonly are ACE inhibitors, such as benazepril (0.25mg/kg each day), or calcium channel blockers, such as amlodipine besylate (0.625mg total dose every 24 hours). These drugs may be given alone, or if either drug alone is insufficient, they may be given together.

•Treatment aims to keep the mean systolic blood pressure below 180mmHg and ideally approximately 160mmHg.

Figure 4.44 (a) Systemic hypertensive disease in a Domestic Shorthair. In this fairly severe case there are true variations of retinal-vessel calibre. Preretinal haemorrhage is apparent dorsally. Multiple bullous detachments are present as a consequence of subretinal effusion. Mean systolic blood pressure was 280 mm Hg at the time of the photograph. (b) Within a week of initiating treatment to reduce the systemic blood pressure the retina has re-attached and the large preretinal haemorrhage has begun to resorb. Mean systolic blood pressure was 210 mm Hg at the time of the photograph.

Figure 4.45 Systemic hypertensive disease in a Domestic Shorthair. In this blind and severely-affected cat there is extensive intraocular haemorrhage and retinal detachment. The two distinct blood-containing bullae, at approximately 11 and 12 o’clock, indicate haemorrhage from ruptured aneurysms. The more extensive haemorrhage, from 4 o’clock to 8 o’clock, is associated with extensive retinal detachment. The optic nerve head of this eye was obscured by the haemorrhage, but papilloedema was present in the other eye. Mean systolic blood pressure was 360 mm Hg at the time of the photograph.

End-stage retinal degeneration and its differential diagnosis

(Figure 4.46)

Congenital and developmental conditions

• Feline panleucopenia virus infection in foetus

Acquired conditions

•Inherited progressive retinal atrophy

•Taurine deficiency retinopathy

•Post-inflammatory chorioretinopathy

•Retinotoxicity

•End-stage glaucoma

•End-stage systemic hypertension

FELINE OPHTHALMOLOGY

FELINE OPHTHALMOLOGY

Figure 4.46 Panretinal degeneration and optic atrophy. The cause was unknown in this cat, the condition was bilateral and severe vascular attenuation and intense tapetal hypereflectivity are notable features.

Haematological disorders associated with retinal haemorrhage

•Anaemia, especially when profound, may be associated with haemorrhage and is also a cause of bullous detachments. Retinal vessels (and choroidal vessels if visible) will be pale

•Coagulopathies and vasculopathies

•Myeloproliferative and myelodysplastic disorders

•Platelet defects such as thrombocytopaenia

Hyper viscosity syndromes

Vessels, especially retinal veins and venules, appear engorged and tortuous. If cyanosis is also present their colour will reflect this, as will the colour of the visible mucous membranes.

•Raised plasma proteins (e.g. FIP)

•Increased red cells (polycythaemia)

•Increased white cells (leukaemia)

Lipaemia retinalis (Figure 4.47)

•Chylomicron-rich blood (circulating triacylglycerides exceed 25mmol/l) imparts a tomato-soup to creamy appearance to the blood column in retinal vessels

•Lipaemia retinalis can be caused by inherited primary chylomicronaemia and chylomicronaemia secondary to disease (e.g. diabetes mellitus)

Figure 4.47 Lipaemia retinalis in a kitten with chylomicronaemia (serum triacylglycerides 41.6 mmol/l). This four week-old kitten was also anaemic because of a heavy flea burden.

NEURO-OPHTHALMOLOGY

Most complex neurological problems in cats require referral for comprehensive investigation.

Feline dysautonomia

This is an autonomic polygangliopathy and any ocular involvement will be bilateral. The commonest ocular feature is widely-dilated non-responsive pupils and there may also be prominent third eyelids and reduced tear production. Generalised signs include depression, anorexia, weight loss, dry mucous membranes, megoesophagus, intermittent regurgitation, constipation, ileus, urinary retention and bradycardia.

Management

•Patients require long-term nursing and avoidance of stress

•Complete recovery may not occur and relapses are possible

Anisocoria

Anisocoria is common in cats and may be of CNS (e.g. inflammation or neoplasia) or ocular origin (e.g. Horner’s syndrome).

Temporary Horner’s syndrome is common after bulla osteotomy and may also be seen after aural administration of ototoxic agents (Figure 4.48).

FELINE OPHTHALMOLOGY