Ординатура / Офтальмология / Английские материалы / Notes on Veterinary Ophthalmology_Crispin_2005

EQUINE OPHTHALMOLOGY

Figure 7.28 (a) Acute equine uveitis as a consequence of a penetrating injury. The eye shows the classical signs of ocular pain. It is also reddened, aqueous flare is present and iris details are not apparent. The single most useful ocular sign of the acute iritis is intense pupillary constriction. Hyphaema marks the track of penetration and may indicate a retained foreign body. (b) The situation remains unclear, even after the haemorrhage had cleared. Note that application of combined topical atropine 4% and phenylephrine 10% has failed to dilate the pupil.

Diagnosis

Non-traumatic aetiology

•A careful and accurate case history should be taken, including any previous and current treatment. Thorough physical examination is required, and neurological function may also need to be assessed

•Examination of both eyes and their adnexa (orbital, paraorbital, eyelids and lacrimal system) must be meticulous, so that normal lighting and darkness will both be needed, as well as a penlight, some form of magnification, indirect and direct ophthalmoscopy

•Systemic sedation/analgesia and an auriculopalpebral nerve block may be necessary if the eye is painful, or if there is any doubt as to the integrity of the globe

•Relevant laboratory investigations (in most cases routine haematology, urea, enzymes, total protein, protein electrophoresis, faecal analysis for parasites and urinalysis)

•Serology (paired samples) should also be undertaken if a microbial cause is suspected, particularly for leptospirosal and viral antibodies

•If necessary, a conjunctival biopsy (e.g. in suspected onchocerciasis) and aqueous and vitreous paracentesis can be incorporated into the diagnostic work-up

Traumatic aetiology

•Blunt trauma is usually more damaging to the globe than penetrating injury, as the intraocular contents can be severely disrupted. Autoimmune uveitis may follow local release of potentially autoantigenic intracellular material when there is cellular damage. The prognosis after blunt injury is usually guarded to poor.

•Penetrating trauma is not uncommon in horses, and may involve entry via the cornea, limbus or sclera with or without direct injury to the iris and lens. Elective procedures such as corneal and intraocular surgery will also be associated with breakdown of the blood–aqueous barrier and consequent uveitis.

•Recurrent bouts of uveitis can follow traumatic injury, especially when uveal tissue is incarcerated in the wound, when there is leakage of lens material, when necrotic tissue is present, when haemorrhage persists, or when foreign bodies remain.

•Penetration of the lens can result in phacoclastic uveitis, which carries a poor prognosis, particularly if it is not recognised and treated aggressively in the early stages.

•The clinical signs of acute lens rupture include pain, blepharospasm excessive lacrimation, evidence of corneal penetration, aqueous flare, lens material in the anterior chamber, focal cataract and an intraocular pressure that is lower than normal.

•If uveitis cannot be controlled after traumatic injury, the eye may eventually become phthitic, a common sequel to serious ocular insult in the horse.

•Other findings in chronic trauma-related uveitis include corneal opacification, pigmentation and vascularisation, hypotony and blindness.

Key features of examination and diagnosis

•The examiner must ascertain that the globe is intact before the eyelids and globe are manipulated as part of the ocular examination.

•If aqueous leakage is a possibility, topical fluorescein (2%) should be used for Seidel’s test – the escaping aqueous dilutes the fluorescein and causes it to fluoresce. This test is easier to interpret if the eye is examined in the dark with a blue light.

•If corneal ulceration is suspected, topical fluorescein (1%) should be used to check for uptake of the stain by the corneal stroma. The eye should be gently irrigated with sterile saline to remove excess fluorescein before checking for fluorescein uptake with a blue light in the dark.

•Ultrasonography may be needed to aid diagnosis if adequate intraocular examination cannot be performed.

•Radiography may be needed if there is any suggestion of orbital or periorbital damage.

Clinical features of acute equine uveitis (Figures 7.28(a,b) and 7.29(a,b))

•Pain, blepharospasm, lacrimation and genuine photophobia*

•Apparent enophthalmos – the painful eye is actively retracted, the third eyelid may be prominent and the upper eyelid lashes will be directed more downwards than normal

•Eyelid oedema may be present, as may chemosis

•Corneal oedema (especially near the limbus) and neovascularisation (an early response in horses)

•Eye may be reddened as a consequence of inflammatory hyperaemia (conjunctival and ciliary injection, particularly towards the limbus), but not necessarily so

EQUINE OPHTHALMOLOGY

EQUINE OPHTHALMOLOGY

Figure 7.31 Chronic equine recurrent uveitis. The eye is quiet, but severely damaged by previous recurrent episodes. There is marked darkening of the iris, degeneration of the granula iridica, an irregular pupil, posterior synechiae, iris rests, secondary cataract and the eye is blind.

Management of uveitis

Complete resolution is achievable in some cases if early treatment is given the first time uveitis occurs and when the cause is readily identifiable (e.g. trauma). However, the prognosis in traumatic cases is guarded when there is extensive intraocular haemorrhage and/or disruption of the intraocular contents. The prognosis is also guarded when there have been previous episodes of inflammation, and the prognosis for restoration of normal visual function is very poor in chronic recurrent cases. Once vision is permanently lost, the only consideration is provision of adequate pain relief and this may be most readily achieved by removal of the globe.

The horse should be walked twice daily in dim light, and, in addition to the usual principles of animal management, vital signs should be monitored. It is important to be aware of any potential undesirable side effects of treatment.

•When uveitis is confirmed, house the affected animal in a dim, quiet and clean environment

•Dust and insects should be kept to a minimum (e.g. feed wet hay at ground level, avoid dusty bedding, control insects)

•Place a subpalpebral lavage device or similar at the time of the initial examination, preferably before sedation/analgesia and local nerve blocks have worn off

•Collect the requisite samples before treatment is started

•Any ocular discharge should be cleaned away before medication is applied

•Petroleum jelly should be applied to the face beneath the lower eyelid to avoid

scalding from excessive lacrimation and to protect from the effects of frequent medication

•Institute medical treatment promptly while investigations as to aetiology are in progress

•The response to treatment can often be gauged within an hour of commencing the combination of topical mydriatic cycloplegic and corticosteroid and systemic non-steroidal anti-inflammatory drugs

•The eye must be re-evaluated at regular intervals

Treatment

Topical

Mydriatics

A mydriatic cycloplegic (atropine sulphate 1–4%) should be applied with sufficient frequency to achieve and maintain mydriasis. This means that the drug is given intensively in the early stages of treatment, and once the pupil has responded it is only given as needed to maintain mydriasis (probably once daily). A directly-acting mydriatic such as phenylephrine hydrochloride 10% may be used in conjunction with atropine in an attempt to disrupt established synechiae.

If there is no pupil response to this two-drug combination within six hours of frequent applications, it is unlikely that successful mydriasis will be achieved. Treatment can be stopped when the eye is free of any signs of pain or inflammation. Owners should be advised that pupillary dilation may persist for up to four weeks after treatment has stopped.

Precautions – topical atropine may cause ileus and subsequent colic, especially in foals, and should only be used with sufficient frequency to maintain pupil dilation. If necessary, intestinal sounds can be monitored, but there is unlikely to be a problem if applications are not given more frequently than every six hours and atropine ointment is always an option in foals.

Corticosteroids

Topical prednisolone acetate 1% is the drug of choice, as it has excellent powers of intraocular penetration. It can be applied every 30 minutes for the first two hours and then every 2–4 hours for the next two days, tapering off to 3–4 times daily if the response is positive. The aim is to cease treatment approximately two weeks after clinical signs have resolved. Topical corticosteroids may be supplemented with lessfrequent subconjunctival injections using 10–40mg methylprednisolone acetate if frequent topical application is not possible.

Precautions – topical and subconjunctival corticosteroids are contraindicated when there is corneal ulceration or abrasion.

Non-steroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory drugs (NSAIDs) are not as potent as corticosteroids and are more expensive. They may be added to a corticosteroid-based topical treatment regime in resistant cases. Ketorolac trometamol 0.5% and flurbiprofen sodium 0.03% every 6–12 hours are the drugs of choice.

Precautions NSAIDs should be used with caution and with regular reassessment when ulcerative keratitis is present.

EQUINE OPHTHALMOLOGY

EQUINE OPHTHALMOLOGY

Antibiotics

Topical antibiotics are only required if intensive and prolonged corticosteroid therapy encourages opportunistic bacteria.

Systemic

Non-steroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory agents such as flunixin meglumine have proved of value as part of non-specific uveitis treatment. Initially flunixin meglumine can be given intravenously at a dose rate of 1mg/kg body weight every 12 hours for 3–5 days. Flunixin meglumine can also be given at the same dose rate orally and intramuscularly. Ketoprofen can be used as an alternative to flunixin meglumine at a dose rate of 2mg/kg every 24 hours for 3–5 days.

Follow-up treatment is given at the minimum effective dosage and can be effected with intravenous or oral dosage of flunixin meglumine (0.25–0.5mg/kg twice daily) or other prostaglandin inhibitors like phenylbutazone (3–5mg/kg twice daily). In cases that relapse, prolonged oral administration of acetylsalicylic acid (aspirin) at a dose rate of 15mg/kg may be helpful, but it is not usually selected for acute cases.

Precautions – NSAIDs can produce gastrointestinal ulceration and haemorrhage and renal damage. These effects can be potentiated by concurrent use of corticosteroids.

Corticosteroids

Steroidal anti-inflammatory drugs can be used as well as, or instead of, the non-steroidal type, always providing that their use is not contraindicated. If both types of drug are given simultaneously there is an increased risk of gastrointestinal haemorrhage. Prednisolone is the drug of choice at a dose rate of 0.5–1.0mg/kg per day for 5–7 days reducing thereafter. Dexamethasone (intramuscular dose rate of 10–40mg/day) is more likely to be associated with undesirable side effects. Corticosteroids should be administered with caution in animals predisposed to laminitis.

Precautions Systemic corticosteroids can cause immunosuppression, laminitis and iatrogenic Cushing’s syndrome. They should be used with appropriate cover if infection is present and with considerable care, or not at all, if corneal ulceration is present.

Antibiotics

If a specific cause for the uveitis is identified, then therapy can be targeted pharmacologically (e.g. parenteral penicillin-streptomycin may be selected if Leptospira titres are rising).

New therapeutic options under investigation

Cyclosporin

Cyclosporin is a non-cytotoxic immunosuppressive cyclic peptide that blocks the transcription of the cytokine interleukin-2 (IL-2) and therefore decreases the responsiveness of T-cells to inflammatory stimuli. The drug may therefore be of value in blocking the non-specific activation of T-cells in recurrent episodes of ERU.

Topical cyclosporin is hydrophobic and so does not penetrate the eye well enough to achieve effective intraocular levels. Intravitreal implantation of a sustained-release cyclosporin delivery device has been assessed in horses with experimentally-induced

EQUINE OPHTHALMOLOGY

Figure 7.32 Iris melanoma. There is extensive iris involvement in this case.

GLAUCOMAS

Intraocular pressure is dependent on the balance between production and outflow of aqueous humour. Glaucoma is the result of imbalance between aqueous humour production and outflow that causes an increase of intraocular pressure above that which is compatible with normal function of the retinal ganglion cells and optic nerve. Glaucoma is rare in horses and suspected cases are best referred.

As outlined in Section 3 (pp 146–151), glaucomas in all species are usually grouped into primary, secondary and congenital types. In primary glaucoma there is no overt ocular abnormality to account for the increase in intraocular pressure (IOP), and this type has not been reliably confirmed in the horse. Secondary glaucomas are the commonest encountered in horses and have an identifiable cause, such as intraocular inflammation, neoplasia or lens luxation. Congenital glaucoma has been reported in foals and is associated with developmental anomalies of the iridocorneal angle (goniodysgenesis).

Horses older than 15 years of age and Appaloosas are at increased risk of developing glaucoma, although it has been reported in a number of other breeds including Thoroughbreds, Arabs and Welsh ponies. The presence of active or inactive uveitis appears to be a major risk factor. Anterior uveitis often leads to the formation of pre-iridal fibrovascular membranes that may limit aqueous absorption by the uvea, and cause physical and functional obstruction of the iridocorneal angle with inflammatory cells and debris.

In horses, the importance of the conventional pathway (whereby aqueous humour passes through the pupil, into the anterior chamber and exits via the trabecular mesh-

work of the iridocorneal angle and associated outflow channels) is matched by the unconventional pathway of uveoscleral outflow (through the iris, ciliary body and sclera). The presence of extensive outflow channels allows aqueous drainage to be maintained in the face of damage to the anterior segment pathways and may explain why glaucoma is a relatively rare sequel to uveitis in the equine eye.

Diagnosis

Glaucoma in horses is being recognised with increased frequency, although the prevalence is surprisingly low (probably less than 0.1%) given the horse’s propensity for ocular injury and marked intraocular inflammatory responses. Diagnosis is made on the basis of clinical signs and measurement of the intraocular pressure.

Tonometr y

•Tonometry is essential to confirm the diagnosis and to monitor the results of therapy. Sequential measurements of intraocular pressure are recommended as there are diurnal variations in normal eyes, and, in addition, horses with glaucoma have quite marked fluctuations of IOP during a 24-hour period.

•The normal equine intraocular pressure measured with a TonoPen applanation tonometer ranges from 7–37mmHg, with a mean IOP of approximately 23mmHg.

•An auriculopalpebral nerve block is recommended prior to tonometry in fractious horses, as the results will be more reproducible and accurate.

Clinical signs (Figure 7.33(a,b))

•There is generally a low index of suspicion of glaucoma in horses in the early stages, the pupils are often only slightly dilated and any discomfort is subtle

•Although it is often a bilateral condition, one eye may be affected before the other, so it is common to find that the two eyes are dissimilar

•Corneal oedema may be a presenting feature, and its appearance is slightly variable, ranging from a vertical strip running from dorsal limbus to ventral limbus in the central cornea to pancorneal involvement*

•In chronic cases, subtle bullous keratopathy develops in addition to the stromal oedema, and corneal function can become compromised with eventual multiple superficial erosions and corneal decompensation

•Corneal vascularisation can also be a chronic feature

•The presence and appearance of corneal oedema may well relate to the extent and duration of IOP elevation

•Linear corneal striae (Haab’s striae) indicate stretching and thinning of Descemet’s membrane; the striae appear as faint, grey, parallel lines (snail tracks) and they sometimes branch*

•Mild uveitis is sometimes apparent, particularly of the anterior uvea; the granula iridica may have degenerated

•The pupil is more dilated than usual, and constricts poorly in bright light*

•It is sensible to compare pupil size between the two eyes and between the patient and a normal horse under the same lighting conditions

•The lens may be subluxated or luxated

EQUINE OPHTHALMOLOGY