Ординатура / Офтальмология / Английские материалы / Notes on Veterinary Ophthalmology_Crispin_2005

GENERAL AND CANINE OPHTHALMOLOGY

perivascular cuffing and poorly defined opacities near blood vessels, pre-retinal exudates, vitritis and optic neuritis. Animals with bilateral optic neuritis are blind. Active inflammation is usually less obvious than inactive and is not observed with anything like the same frequency.

Figure 3.68 Active inflammation of the ocular fundus in a Labrador Retriever with distemper. Multiple focal lesions were present in the tapetal fundus of both eyes and the dog also had neurological signs.

Inactive

Inactive post-inflammatory lesions (Figures 3.69 and 3.70) consist of either focal or diffuse changes in the tapetal and non-tapetal fundus. In the tapetal fundus, there may be sharply-demarcated hyperreflective foci of variable size. Pigment-cell proliferation results in pigment placed centrally in such foci. Disseminated inflammation can produce changes in the whole of the tapetal fundus.

In the non-tapetal fundus, focal and, less commonly, diffuse depigmentation is apparent. The blood vessels crossing affected areas are sometimes tortuous and constricted and perivascular pigment may be present.

Other possible findings include retinal detachment, vitreal changes and optic atrophy. Inactive chorioretinopathies are a common finding in many breeds of dog, especially working Border Collies.

Figure 3.70 Inactive inflammation (diffuse chorioretinopathy) of the ocular fundus in a Border Collie. This is the end stage of severe retinal degeneration, irrespective of the cause. In addition to the panretinal degeneration there is gross vascular attenuation and optic nerve atrophy and the eye is blind.

Aetiology and diagnosis

•Establishing the cause of active fundus inflammation is not always easy

•The causes of fundus inflammation have been summarised under Uveitis (this section, pp 132–135)

•Complete physical examination, blood samples (routine haematology, serum proteins, biochemistry and serology) and specific tests, if available, are best undertaken when the inflammation is active

•Imaging techniques are sometimes helpful if the ocular media are cloudy and if retinal detachment is suspected

Treatment

Depends on finding the cause

Retinal detachment

The embryological intraretinal space remains throughout life, and the neuroretina is only loosely attached to the retinal pigment epithelium, so that the two may separate to produce a retinal detachment. The retina is firmly attached (or inserted) at the ora ciliaris retinae and also around the optic nerve head, and the gel-like consistency of the normal vitreous helps to hold the retina in place.

Causes of retinal detachment

Congenital

For example, associated with CEA, RD, PHPV and multiple ocular defects. There is a range of presentations, from congenital non-attachment to detachment.

Traumatic

For example, blunt trauma. Retinal tears may be produced because of the different rates at which the vitreous and the coats of the eye change shape. Retinal tears and holes usually result in a rhegmatogenous detachment.

GENERAL AND CANINE OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

Intraocular problems

For example, the development of fibrous vitreoretinal adhesions following severe inflammation may produce a traction detachment. The retina is also more likely to detach in the presence of severe vitreal degeneration and syneresis.

Intraocular and extraocular space-occupying lesions

For example, choroidal tumours and extraocular tumours can push the retina off, resulting in a solid detachment.

Systemic problems

Systemic hypertension (primary and secondary) is associated with the accumulation of subretinal fluid, which lifts the retina off. Initially there are bullous detachments and later, without treatment, there is total detachment. Detachments as a consequence of systemic hypertension are examples of serous or exudative detachment (Figure 3.71). The subretinal fluid has the composition of a transudate initially, but later may become more exudative in nature.

Systemic hypertension is also associated with changes in choroidal and retinal vasculature and retinal haemorrhage. Causes of secondary systemic hypertension include renal disease, hypothyroidism, hyperadrenocorticism, phaeochromocytoma and diabetes mellitus.

Other causes of serous detachment include the uveodermatological syndrome and severe inflammation (e.g. systemic mycoses and parasitic infections such as toxoplasmosis).

(a)

(b)

Figure 3.72(a,b) Hyperviscosity syndrome in a Toy Poodle with the congenital heart disease tetralogy of Fallot. The external eye (a) and fundus (b) are illustrated. The dog was cyanotic and compensatory polycythaemia was the reason for the hyperviscosity.

Figure 3.73 Autoimmune haemolytic anaemia in an Old English Sheepdog. Note the extreme pallor of the retinal vessels, giving a spurious impression of attenuation.

Retinal haemorrhage (see vitreous haemorrhage, this section, pp 155–158)

OPTIC NERVE

The shape, size and colour of the canine optic nerve head is variable. The variation can largely be related to the age of the animal and the extent of medullation (i.e. nonmyelinated and round in young puppies). The optic nerve head (optic disc, or papilla) is the bulbar portion of the optic nerve. The retrobulbar and cranial portions of the nerve cannot be examined ophthalmoscopically. Congenital anomalies of the optic nerve head are rare and include aplasia, hypoplasia and coloboma.

GENERAL AND CANINE OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

172 Notes on Veterinary Ophthalmology

ACQUIRED ABNORMALITIES OF THE CANINE OPTIC NERVE

Optic neuritis or papillitis (intraocular)

History, ophthalmoscopic signs and diagnosis (Figure 3.74(a,b))

•An uncommon problem which presents as sudden blindness or defective vision. May be unilateral, or bilateral

•Affected eyes are blind during the active inflammation, with an impaired or absent PLR and a fixed dilated pupil

•Optic nerve head appears enlarged and hyperaemic; the normal physiological pit is absent

•Focal haemorrhages may be present within or surrounding the optic nerve head

•Peripapillary retinal oedema or detachment

•May be cellular infiltrates in posterior vitreous

•Normal ERG

Figure 3.74(a,b) Optic neuritis in a Collie Cross with toxoplasmosis. Active stage of inflammation (a) and the same eye after treatment (b). The pathological conus (reflective halo surrounding the optic nerve head) apparent in (b) indicates the extent of the peripapillary oedema during the active phase.

Treatment

See Retrobulbar optic neutritis p. 173.

Aetiology

•Systemic disease, e.g. distemper, toxoplasmosis, leptospirosis

•Local disease, e.g. orbital cellulitis, orbital abscess

•Trauma, e.g. to globe or orbit

•Neoplasia, e.g. retrobulbar neoplasia

•Neurological, e.g. granulomatous meningoencephalitis (GME)

•Toxic and metabolic

•Idiopathic, presumed immune mediated

Retrobulbar optic neuritis (retrobulbar)

Ophthalmoscopic signs

•Uncommon, dilated pupil (unilateral or bilateral) and blindness but the optic nerve head appears normal

•Normal ERG

Differential diagnosis of retrobulbar optic neuritis

•SARD

•Disorders of the central nervous system

Treatment of optic neuritis (both intraocular and extraocular)

•Urgent referral necessary if the diagnosis is in doubt

•Drug treatment for optic neuritis and retrobulbar optic neuritis is the same

•High levels of systemic corticosteroids (usually oral prednisolone at 1–2 mg/kg each 24 hours)

•Rapid response to therapy gives better prognosis than failure to respond, but, for all cases, the prognosis is guarded, as permanent damage occurs rapidly and relapses are common

•Monitor carefully and check for systemic or CNS involvement

•A region of peripapillary hyperreflectivity or even optic atrophy may develop as a sequel to optic neuritis and the animal may recover vision, be partially sighted or blind

Optic ner ve neoplasia

•Primary tumours (e.g. glioma, meningioma, astrocytoma) are rare, but an expanding brain tumour may compress the intracranial optic nerve

•Meningioma is the commonest primary tumour and can involve the optic nerve by primary neoplastic transformation of cells within the optic nerve sheath, or secondary extension of intracranial neoplasia

•Infiltration of the optic nerve by tumour cells can also occur, most commonly in animals with lymphoma

Oedema of the optic ner ve (papilloedema)

Papilloedema is a clinical sign, not a diagnosis, and is usually the result of raised intracranial pressure.

Aetiology

•Congenital or acquired hydrocephalus

•Intracranial and extracranial space-occupying lesions which may be infectious, inflammatory or neoplastic in origin

•Ischaemia (e.g. severe systemic hypertension)

Clinical signs and ophthalmoscopy

•Unusual, affected animals usually have gross neurological signs (e.g. behavioural changes and locomotor problems)

•May be associated with visual disturbance, including vision loss, depending on the aetiology

•Swollen optic nerve head, with an indistinct and elevated margin (Figure 3.75)

GENERAL AND CANINE OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

•May be venous engorgement and increased tortuosity of the retinal vessels. The retinal vessels may deviate as they cross the margins of the optic nerve head

Differential diagnosis

•Differentiate from optic and retrobulbar neuritis

•Differentiate from pseudopapilloedema, a normal variant as a consequence of marked myelination of the optic nerve head that is common in German Shepherd Dogs and Golden Retrievers

•Vision may be affected and so may the pupillary light response, reflecting the underlying aetiopathology, rather than any specific feature of papilloedema

Treatment

Remove the primary cause, if possible

(b)

(a)

Figure 3.75(a,b) Papilloedema in the right eye of a Papillon with a brain tumour in the chiasmal region. Optic atrophy was present in the left eye of the Papillon in Figure 3.75.

Optic ner ve atrophy

•The end stage of severe insults such as inflammation, chronic optic nerve oedema and ischaemia (Figures 3.70 and 3.75(b))

•The changes may not develop for some weeks after the initial insult or disease process

•Optic atrophy is quite frequently a complication of eyeball prolapse, so a suitable guarded prognosis should be given in such cases, even when the eye has been replaced rapidly into the orbit

Ophthalmoscopic signs

The optic nerve head usually appears pale and shrunken (loss of myelin results in a round optic nerve head, rather like that of a puppy or cat) and the eye is blind.