Ординатура / Офтальмология / Английские материалы / Notes on Veterinary Ophthalmology_Crispin_2005

GENERAL AND CANINE OPHTHALMOLOGY

•Meticulous examination of both eyes and their adnexa with adequate magnification is essential

•Check that tear production of both eyes is normal (likely to be excessive, but occasionally it is reduced in the affected eye if tear production is abnormal). The Schirmer tear test is performed before any other preparations are applied to the eye

•Corneal scrapings and swabs for culture should be taken early in the course of disease and before treatment has altered the initial presentation. Topical local anaesthesia is necessary. Sample from the edge of the ulcer, as this is where organisms will be replicating if infection is present

•The results of Gram staining may enable appropriate antibiotic therapy to be selected, but note that Gram +ve organisms are often easily found and may not always be of great significance. Gram -ve organisms are likely to be of significance if any can be found

•It is essential to use ophthalmic stains such as fluorescein to aid diagnosis, but after swabs and scrapes have been taken. Excess stain should be rinsed away with sterile saline and the eye examined as soon as possible after fluorescein application so as to avoid false positives

involved. A faint scar will remain if there has been stromal involvement. Topical antibiotic is not always required, particularly if the cause has been established and eliminated (e.g. ectopic cilium).

•Protection during healing is not usually required, however, a therapeutic soft contact (bandage) lens (TSCL) or third eyelid flap can be used for those cases in which pain

relief and protection are needed. A bandage lens can be put in after applying topical local anaesthetic and the edge of the lens should reach some 2 mm beyond the limbus. The lens may be left in situ for up to six weeks. A general anaesthetic is needed for the placement of third eyelid flaps, and the ulcerative lesion is lesseasily monitored as it is hidden from sight. TSCLs provide a useful and preferable alternative to third eyelid flaps, but should be avoided when there is keratoconjunctivitis sicca, active ocular surface infection, serious eyelid dysfunction, hypoaesthesia (an anaesthetic cornea) or uveitis.

Deep corneal ulceration (loss of approximately half or more of the corneal thickness)

•Deep ulceration may be an immediate result of the initial injury or a later complication. If there is any likelihood of corneal perforation then healing must be aided by support from a graft (e.g. free conjunctival graft, conjunctival pedicle graft, porcine submucosal graft). A rotation conjunctival pedicle graft is the most commonly used means of support (Figure 2.14(a–g), p. 45), as it brings a blood supply direct to the damaged region. It is probably the treatment of choice. The graft is placed with the patient under general anaesthesia and it is usually left in situ for at least four weeks before it is sectioned, following the application of topical local anaesthetic. It is important to warn owners that the graft will become white and necrotic once it has been sectioned and it is axiomatic that sectioning does not take place until healing is complete.

•Full-thickness complications will need primary repair and may also require keratoplasty techniques. Such cases should be referred if microsurgical facilities and expertise are not available.

•Intensive treatment with topical antibiotic solution (proprietary preparation or specially made up fortified solution) will be required for the management of deep corneal ulcers.

•Deep corneal injuries are invariably accompanied by uveitis, and symptomatic treatment of the uveitis with topical atropine sulphate 1% must accompany treatment.

•Anticollagenases, such as acetylcysteine or EDTA, are of largely unproven benefit in the treatment of complicated ulcerative keratitis, and careful removal of necrotic tissue is a more rational approach. Ascorbic acid (vitamin C) has proved useful in human patients for treating the stromal lysis that follows alkali burns and may be given orally. Whole fresh serum is easy to obtain from the patient and is an empirical and readily available topical therapy for any situation where collagenases and proteases complicate the situation. Acetylcysteine (5–10%) may be used in conjunction with fresh serum to prevent collagenolysis.

•If the ulcer progresses despite treatment, the patient is best referred before perforation occurs.

Antibiotic selection

• If bacterial infection is proved or suspected then an appropriate topical antibiotic

GENERAL AND CANINE OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

should be selected. For most Gram +ve infections, topical chloramphenicol can be used; for most Gram -ve infections gentamicin is effective. For mixed infections, a triple preparation containing, for example, polymixin B, neomycin and gramicidin, is useful. For confirmed Pseudomonas aeruginosa infection gentamicin is the drug of choice. On the rare occasions when gentamicin-resistant Pseudomonas aeruginosa infection is encountered, ciprofloxacin can be used

•Topical rather than systemic therapy is always the route of choice for corneal infections

•Ointments and suspensions can be used to treat ulcers with epithelial loss only; they should not be used in situations where they can become incorporated in the healing tissues, or when there is full-thickness perforation

•Proprietary solutions are the treatment of choice for uncomplicated ulcers up to midstromal depth

•Fortified liquid preparations should be reserved for complicated ulcers and for when corneal penetration has occurred (see Appendix 2, pp 333–344)

Points to note in the treatment of ulcerative keratitis

•Local anaesthetics should never be used as part of treatment regimes, as their action is of short duration only and they are epitheliotoxic. If pain is marked then systemic analgesics should be given.

•Topical corticosteroids should not be used to treat ulcerative keratitis as they can adversely affect the reparative functions of epithelial cells and fibroblasts and also enhance stromal collagenolysis. The only exception to this rule is the carefullymonitored treatment of certain rare immune-mediated corneal problems.

•Topical non-steroidal inflammatory agents (e.g. ketorolac trometamol 0.5%) may be used with caution when significant uveitis accompanies ulcerative keratitis. They appear not to cause collagenolysis, but may delay epithelialisation.

Chronic superficial keratoconjunctivitis (pannus)

Aetiology

•An immune-mediated problem

•Certain breeds are susceptible, most commonly the German Shepherd Dog, but also Belgian Shepherd Dog, Border Collie, Dachshund and gaze hounds such as the Greyhound and Lurcher

•Predisposing factors include ultraviolet light, altitude and smoke

Clinical findings

•In the UK, dogs first present with pannus at approximately 3–5 years of age

•The condition usually produces mild ocular discomfort

•Some or all of the conjunctival limbus (follicular hyperplasia), cornea (initially inferotemporal/ventrolateral pink-grey fibrovascular infiltration, but will extend across the whole cornea if untreated) and third eyelid (follicular hyperplasia with depigmentation) may be involved (Figure 3.30)

•Involvement of the third eyelid alone is sometimes separately classified as plasmacytic conjunctivitis, a plasma cell infiltrate, or plasmoma, but it is treated in the same way as pannus. The condition is usually bilateral

•Corneal pigmentation and lipid deposition may complicate the presentation, but corneal ulceration is not usually present

•Note that the roughened nature of the infiltrate can lead to false positives after fluorescein application unless excess stain is rinsed away gently with saline or water

•Pannus is essentially a superficial, subepithelial, fibrovascular infiltration in which lymphocytes and plasma cells predominate

Treatment

•The clinical appearance can be largely reversed by topical application of cyclosporin. Topical cyclosporin ointment 0.2% applied once or twice daily is the treatment of choice, especially as it appears to reduce the degree of corneal pigmentation. A side effect of no clinical relevance is that it will also increase tear production.

•A surface-active preparation such as fluorometholone, or other topical corticosteroid such as prednisolone, betamethasone, or dexamethasone, can also be used in the early stages of treatment to achieve a quick resolution of clinical signs. For example, the corticosteroid preparation should be applied at least five times daily for five days, then four times daily for four days, then three times daily for three days, then two times daily for two days, then once daily for one day. Long-term topical corticosteroids are not usually indicated and cyclosporin can be introduced as the dose of corticosteroid is tapered off.

•Note that recurrence is likely when either of the above treatment regimes is stopped, almost universally so in the commonly-affected susceptible breeds. In most cases, therefore, treatment should be maintained for life once the diagnosis has been made. The treatment regime is varied to take into account known predisposing factors such as ultraviolet light.

•Surgery (superficial keratectomy) is required only in the very rare instances of those dogs that remain blind despite medical therapy, usually because of extensive pigment deposition. Topical treatment should be started as soon as possible after surgery to prevent rapid reversion to the preoperative state.

GENERAL AND CANINE OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

in the remainder, there are no discernible abnormalities. Additional factors, such as distichiasis, may modify the local appearance.

In some breeds the condition is likely to be inherited, and in others a familial tendency is demonstrable. Crystalline stromal dystrophy may be a consequence of an inherent metabolic defect in the corneal fibroblasts, possibly a temperature-dependent enzyme defect, and slit-lamp examination with maximum magnification often indicates panstromal accumulation of lipid material in the fibroblasts. The grossly apparent axial and paraxial crystalline appearance is associated with fibroblast death and liberation of the accumulated lipid material.

It should be noted that the central cornea is more than 3°C cooler than the peripheral cornea, so the central cornea would be preferentially affected by a temperaturedependent enzyme defect.

Figure 3.31 Crystalline stromal dystrophy in a Cavalier King Charles Spaniel. Both eyes were affected. Note the typical crystalline appearance and axial position of the gross lesion. The dog was normolipoproteinaemic.

Lipid keratopathy

Lipid keratopathy (Figure 3.32) is the deposition of lipid within the cornea of one or both eyes. The appearance is very variable. Vascularisation is a constant feature of lipid keratopathy and it may precede or follow the predominantly-stromal lipid deposition. Lipid keratopathy may be a complication of ocular inflammation, and some affected animals, but by no means all, have plasma hyperlipoproteinaemia (usually raised high density lipoprotein cholesterol).

Figure 3.32 Lipid keratopathy in a Golden Retriever that had been scratched by a cat when he was a puppy. The eye had subsequently become phthitic. Low intraocular pressure is one of many factors that can enhance lipid deposition, and phthitic eyes have very low intraocular pressure. The dog also had mild hyperlipoproteinaemia (mainly affecting cholesterol).

Arcus lipoides corneae (corneal arcus)

Arcus lipoides corneae or corneal arcus (Figure 3.33(a,b)) is bilateral peripheral corneal lipid deposition. The condition in dogs is always associated with plasma hyper-

(a)

lipoproteinaemia, most commonly secondary to a problem such as primary acquired hypothyroidism.

Figure 3.33(a,b) Arcus lipoides corneae (corneal arcus) in a Rottweiler. The dog had primary acquired hypothyroidism and was hyperlipoproteinaemic (both cholesterol and triacylglycerides were raised). Peripheral lipid deposition was present in both eyes, but the right eye (a) was first to become involved, and the lipid has a more crystalline appearance than that of the left eye (b).

Management of corneal lipid deposition

•As local and systemic factors can be involved, both must be considered in assessing the management options. In general, progressive corneal opacification, any indications of active ocular inflammation, any ocular manifestations of hyperlipoproteinaemia (e.g. lipaemic aqueous, lipaemia retinalis), or any signs of systemic disease, are indications for detailed investigation

•The total serum or plasma cholesterol and triacylglyceride levels and lipoprotein profile should be analysed. Total cholesterol and triacylglyceride values alone provide insufficient information

•Systemic disease should be diagnosed and treated

•Dietary manipulation (e.g. low fat, high fibre) may be used to modify the evolution of the corneal opacity if no other abnormalities are established. Most of the lipidlowering drugs currently used in human medicine are not applicable to management of dyslipoproteinaemia in the dog

•Any ocular inflammation must also be investigated and treated, as should any potential exacerbating factors such as distichia

•Other factors that may affect the potential for lipid deposition, but are not amenable to treatment, such as ocular hypotension (reduced intraocular pressure) must be taken into account

OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

muscle is located in the pupillary portion of the stroma. Two layers of epithelial cells form the posterior part of the iris. The anterior epithelium consists of an epithelial apical portion and a muscular basal portion, the iris dilator muscle, which projects into the iris stroma. The posterior surface of the iris consists of very heavily pigmented epithelial cells. Iris musculature and the epithelial layers are of neuroectodermal origin, and the stroma is of mesenchymal origin.

Iris colour depends on the number of melanocytes in the stroma and the thickness of the anterior border layer. The anterior surface is grossly divisible into a central (pupillary) zone and a peripheral (ciliary) zone, separated by the collarette. The pupillary zone of the iris is usually darker and thinner than the ciliary zone and the differences are obvious in most dogs.

Control of pupil size

The main function of the sphincter and dilator muscles is to control pupil size under different lighting conditions. The sphincter muscle encircles the iris at the pupillary zone and pupil constriction is mediated by the parasympathetic branches of the oculomotor nerve. Pupillary constriction regulates the amount of light that enters the eye, increases the depth of focus for near vision and reduces optical aberrations.

The dilator muscle controls pupillary dilation and consists of radially orientated fibres that pass from close to the pupil towards the root of the iris. Dilation is mediated by postganglionic sympathetic nerves.

ANATOMY AND PHYSIOLOGY OF THE CILIARY BODY

The ciliary body is located posterior to the iris and anterior to the choroid and is roughly triangular in cross section, its base facing the anterior chamber and its apex merging with the choroid. The ciliary body can be divided into the pars plicata and pars plana, the latter extending to the edge of the retina, a zone known as the ora ciliaris retinae. The stroma, ciliary muscles and blood vessels are of mesenchymal origin, the epithelium originates from neuroectoderm. The ciliary body serves to anchor the zonular fibres of the lens. Ciliary muscles are poorly developed in domestic animals and there is little dynamic accommodation of the lens in consequence.

Aqueous production

Aqueous is produced from the non-pigmented epithelium of the pars plicata of the ciliary body. The rate of aqueous production equals that of outflow, thus maintaining a relatively constant intraocular pressure.

ANATOMY AND PHYSIOLOGY OF THE CHOROID

The choroid, a highly-vascularised structure, is situated between the retina and the sclera. The energy requirements of the outer retina are served by diffusion of glucose and oxygen from the choriocapillaris vessels. The outer retina is exposed to near arterial levels of oxygen because of the high rate of blood flow through the choroid.

The choroid consists of:

1A poorly-developed basal complex known as Bruch’s membrane, adjacent to the retinal pigment epithelium

2The choriocapillaris, a network of highly fenestrated capillaries, linked to the large vessels of the stroma

3A cellular tapetum located in the dorsal choroids, which increases visual sensitivity by reflecting light back through the photoreceptors. The fine vessels (choroidal arterioles) that traverse the tapetum to link the blood vessels of the stroma and the choriocapillaris are such an obvious feature of fundus examination that they are referred to as the ‘stars of Winslow’

4The stroma (fibrocytes, melanocytes, elastic fibres and collagen fibres) and blood vessels

5The suprachoroidea (heavily-pigmented connective tissue) adjoins the lamina fusca of the inner sclera

CONGENITAL AND DEVELOPMENTAL ABNORMALITIES OF

THE IRIS

Colour variations

Normal variations in the colour of the iris are common in dogs of different breeds and coat colour. Some of these variations are illustrated later together with photographs of the normal fundus. The two eyes of the same animal may differ and there may also be variations of colour in the same eye. Colour differences are termed heterochromia. Ocular heterochromia may be the only manifestation of colour dilution, or may be part of more widespread colour dilution, especially in merle animals. Sub-albinism refers to a lack of normal pigmentation and manifests as a blue iris. It is reasonably common in dogs.

Congenital colour variations should be distinguished from acquired ones – in patients with chronic or previous uveitis it is common for the iris to become darker and lose fine structural detail.

Merle animals

A range of ocular abnormalities may be encountered in merle animals of any species. Mildly-affected animals have heterochromia and iris hypoplasia (incomplete iris development) often with abnormal pupil position (correctopia) and shape (dyscoria). Persistent remnants of the pupillary membrane and iris colobomas are also common. Severe ocular defects, often multiple in nature, are more likely to be encountered in animals which are homozygous for the merle trait; they include microphthalmos, retinal dysplasia, optic nerve hypoplasia and cataracts. Affected animals are also likely to be congenitally deaf. The combination of a white coat, blue eyes and deafness in animals is analogous to Waardenburg’s syndrome in humans.

Persistent pupillar y membrane

Persistent pupillary membrane (PPM) is the most obvious and common example of faulty differentiation of the anterior segment, and is a result of failure of the normal process of atrophy of the vascular arcades (tunica vasculosa lentis anterioris) and associated mesenchymal tissue (Figure 3.34). Remnants of the pupillary membrane may be

GENERAL AND CANINE OPHTHALMOLOGY

GENERAL AND CANINE OPHTHALMOLOGY

found as an isolated defect or in conjunction with other abnormalities (anterior segment dysgenesis and multiple ocular defects). Persistent pupillary membrane may be inherited in the Basenji and possibly in other breeds.

Figure 3.34 Persistent pupillary membrane in a cross-bred puppy. Note that the remnants arise, predominantly, from the iris collarette.

Clinical features

Persistent pupillary membrane remnants often arise from the collarette region of the iris. They may run across the face of the iris ± span the pupil ± attach to the anterior lens capsule ± attach to the posterior cornea. They should be distinguished from acquired adhesions (synechiae).

Incomplete iris development

There is a range of appearances, from apparent absence of the whole iris (aniridia) which is very rare, to incomplete iris development (hypoplasia) or absence of a portion of the full thickness of the iris (coloboma) which are uncommon (Figure 3.35). Iris hypoplasia and colobomatous defects should be differentiated from acquired iris atrophy.

ACQUIRED ABNORMALITIES OF THE UVEAL TRACT

Iris pigmentation

Discrete hyperpigmentation and pigment proliferation on the iris surface can occur as a phenomenon of ageing and is usually of no clinical significance in such cases (Figure 3.36). However, all unexplained changes of pigmentation should be observed carefully over time, as it is not usually possible to differentiate focal pigmented lesions on the basis of a single clinical examination alone. Malignancy may be associated with proliferation, elevation and iris infiltration. Iris freckles are of no clinical significance and consist of focal accumulations of normal, but hyperplastic, melanocytes. Iris nevi represent proliferations of abnormal melanocytes and are of significance as they can undergo malignant transformation. Iris neoplasia, most commonly melanoma, should always be considered in the differential diagnosis; malignancy is associated with rapid enlargement.

Figure 3.36 Benign melanosis in a Labrador Retriever. Note the superficial nature of the pigment.

In breeds such as the Cairn Terrier diffuse ocular melanosis, associated with proliferation of melanocytes, is recognised as a breed-related problem in middle-aged and older dogs. The large numbers of pigment-laden cells that accumulate can cause an insidious secondary glaucoma and the prognosis for retention of long term vision is poor (Figure 3.37).

GENERAL AND CANINE OPHTHALMOLOGY