opthamology Flashcards Preview

Integrated Clinical Dog and Cat > opthamology > Flashcards

Flashcards in opthamology Deck (194)
0

What are external hordeolum?

styes - young dogs, may have single or multiple abscesses caused by suppurative infection of the glands of zeiss or moll. treatment is the same as for meibomianitis.

1

What is chalazion?

Obstruction of the tarsal gland secretions by a blocked duct can cause the gland to rupture, liberating its content within the eyelid substance, visible through the palpebral conjunctiva as a firm spherical, yellow lipogranuloma. If Occular surface irritation is present then treat by incising into the lesion with a blade, under general anaesthesia and curetting out the contents, followed by topical antibiotics for 7-10 days.

2

What happens to the eyelids after trauma?

Marked oedema comon. repair carefully without undue delay, ensuring good apposition at the lid margins. minimal debridement is required because of the good vascular supply to the lids. if laceration is extensive then repair in two layres, ensuring the deeper layer does not go full thickness through the conjunctiva where it will abrade the cornea.

3

Describe eyelid neoplasias

Most lid tumours occur in old dogs and are benign in behaviour. tarsal gland adenomas are most common followed by melanomas. they grow slowly but may abrade the cornea or bleed. The lid margin should be closed first and the figure of 8 suture is a neat way of taking the knot of the first suture away from the lid margin.

4

What is the third eyelid?

The third eyelid is a large fold of conjunctiva supported internaly by a T shaped cartilage. the base of the cartilage is surrounded byt he nictitans gland, which produces 40% of the aqeous component f the preocular tear film. The third eyelid is important in the distribution of the tear film. it is swept across the eye when the lids are closed in blining. the TEL is devoid of muscle in the dog, so its position is determined by the size and position of the globe. In the cat - movement can be both active and passive.

5

Describe prolapse of the nictitans gland

Appears acutely as a smooth pink swelling at the medial canthus. the mass is seen to protrude from behind the leading edge of the membrane. Thought to result from a weakness in the connective tissue attachment between the gland and the peroorbital tissue. Unacceptably high risk of dry eye if gland is excised. Surgical replacement should therefore be attempted. Pocket eye technique and anterior anchoring technique useful.

6

What is scrolling of the third eyelid?

Also known as eversion or kinking of the cartilage, thee straight stem of cartilage kinks, forcing the membrane to fold outwards so that the leading edge no longer contacts the cornea. may have some Occular discharge and conjunctivitis. treatment is by excising the kinked portion of the cartilage from the deep surface of the membrane.

7

What is plasma cell infiltration of the third eyelid?

Affects GSD and collie types, with bilateral depigmentation of the membrane, a pink/red fleshy infiltrate and rough irregular surface. The infiltrate consists of plasma cells and lymphocytes and is often concurrent with chronic superficial keratitis. Despite its appearance there is usually minimal disconfort. Treatment is with topical corticosteroids frequently initially reducing to a maintenance dose.

8

How do foreign bodies affect the third eyelid?

The deep surface is an occasional site for a foreign body that may be easily missed. the clinical signs are acute and marked discomfort, frequently with corneal damage opposite the foreign body. sedation and topical anaesthesia usually required to identify and remove it.

9

What conditions may cause third eyelid protrusion?

REtrobulbar space occupying lesions with exopthalmos eg extraconal abscess or tumour. REtraction of the globe with enopthalmos. Micropthalmos or phthisis bulbi - reduction in orbital contents. Dehydration, cachexia, masticatory muscle atrophy. alteration to nervous control- horners syndrome.

10

Describe the clinical anatomy of the conjunctiva

It is a thin mucous membrane. it extends from the lid margins where it is continuous with the epidermis to the limbus where it meets the cornea epithelium. It lines the inner surface of the upper and lower lids, reflected forwards at the fornixes as the bulbar conjunctiva over the globe. it is mobile, has a good blood supply and heals rapidly. The conjunctiva contains goblet cells, contributing the mucous fraction of the tear film and lymphoid follicles.

11

What is conjunctivitis?

The whole conjunctiva becomes diffusely reddened with a variable amount of discharge. In significant bacterial infections the discharge has a typically purulent apearance. Interpretation of bacterial culture complicated by he fact conjunctiva is not sterile and has a wide range of bacteria. Mostly commensals recovered eg streptococci, staphylococci, occasional gram -ves.

12

How does bacterial conjunctivitis occur?

The majority of cases are secondary to causes such as an eyelid mass, eyelid irregularity or foreign body. primary bacterial conjunctivitis is less common, acute and self limiting. in both situations a mucopurulent Occular discharge occurs in the presence of increased or normal tear production. Infection frequently wth staph or other gram positives. Fusidic acid has god activity against gram positives - apply once or twice daily.

13

What is opthalmia neonatorum?

Infection within the conjunctival sac before the eyelids are opened (usually at 10-14 days) will cause swelling of the eyelids, sometimes with a small amount of pus escaping at the medial canthus. this must be treated promptly to avoid corneal ulceration and penetration. the lids should be opened along their line of fusion digitally or with blunt ended scissors. after culture the occular surface should be irrigated with sterile saline and the infection treated with broad spectrum, topical antibiotic ointment and frequent application of occular lubricants.

14

What is ectropion?

Can cause a mild conjunctivitis due to exposure. Lid shortening can be considered in the worst affected cases, otherwise client education only.

15

How does distemper affect the eyes?

A purulent Occular discharge may accompany the other signs of the disease. Treatment is symptomatic, check tear production as the virus attacks the lacrimal gland, possibly leading to corneal damage. A chorioretinitis may also be present.

16

What is follicular conjunctivitis?

Hypertrophy of the lymphoid follicles scattered on the bulbar surface of the Nictitans and the conjunctival forniixes, occurs with chronic antigenic stimulation. The condition is poorly understood, but clinical signs are usually mild, occurring most often in dogs <18 months old. Most cases respond to treatment with saline irrigation and symptomatic use of topical steroids. Non responsive cases may improve following mechanical debridement of follicles following topical anaesthesia using a dry gauze placed over a cotton bud.

17

How does allergy affect the conjunctiva?

Conjunctiva and lids may be involved in local allergic reactions or generalised atopy. the finding of a single eosinophil on conjunctival cytology is considered diagnostic of an allergic process, although plasma cells and lymphocytes are more common. Intermittent use of topical steroids may be required. (alternatively topical antihistamines or mast cell stabilisers may be required). Immediate hypersensitivity reactions are occasionally encountered with rapid and dramatic chemosis (conjunctival oedema). These are usually self limiting once the dog is no longer in contact with the allergen and most respond well to a single parenteral dose of short acting corticosteroids.

18

What is chronic conjunctivitis?

A low to medium grade mucopurulent chronic conjunctivitis is sometimes seen as part of a generalised problem in association with marginal tear production, seborrhoea, pyoderma, otitis externa, ectropion etc, particularly in cocker spaniels. treatment is symptomatic with a view to control rather than cure. Topical cyclosporin ointment can make a considerable difference in those cases where tear production is marginal.

19

Describe the canine lacrimal system?

The lacrimal system consists of 3 components - secretory - glandular production of the lipid, aqueous and mucus layers of the preocular tear film. Distributory - movements of the eyelids and nictitans distribute the tear film over the Occular surface. Drainage - drainage of tears to the nasal cavity via the nasolacrimal syste.

20

What is keratoconjnctivitis sicca?

A common condition in the dog resulting from a deficiency in the aqueous portion of the tear film produced by the lacrimal and nictitans glands. Causes are immune mediated destruction of lacrimal tissue, with progressive loss. Seen in westies, cocker and CKCS, shih tzu and lhaso apso. Also caused by endocrine diseases (hypothyroidism, diabetes mellitus, hyperadrenocorticism) or drug induced - sulphadiazine (Widely used in sulphonamide antibiotic, found in tribrissen) and sulphasalazine may cause acute dry eye in the dog. The cornea may be ulcerated. drugs should be discontinued. damage may be temporary or permanent Viral adenitis - inflammatory destruction of lacrimal tissue in distemper. Unilateral KCS is less common. Causes include excision or uncorrected prolapse of the TEL, topical atropine, congenital abscence or hypoplasia of lacrimal tissue, neurological deficits, orbital disease.

21

What are the clinical signs of keratoconjunctivitis Sicca?

Conjunctivitis, mucopurulent discharge characteristically tenaceous, lustreless cornea with more advanced disease, variable degrees of corneal neovascularisation and pigmentation. Test with schirmer tear test strips - The mean normal STT is around 21mm in the dog. Values of 13-15mm should be interpreted on the basis of the occular surface appearance and level of discomfort. Treated with tear replacement - lubrithal gel, lacrilube, hylashield or tear stimulation with topical 0.2 cyclosporine ointment. Tacrolimus or pimecrolimus can be used if cyclosporine response is inadequate. Oral pilocarpine may be used in neurogenic cases with denervation hypersensitiviity. Surgical parotid duct transposition used to be performed frequently but now reserved for refractory cases - may be deposition of irritant calcium crystals on the cornea.

22

How can epiphora be investigated?

Epiphora is overflow tears due to poor drainage. Check with fluorescein instilled into both eyes and observe external nares for passage of fluorescein. Lack of dye does not necessarily mean that drainage is inadequate as false negatives are common. Nasolacrimal cannulation - can be performed under topical anaesthesia and a sedation in many dogs, upper punctum is cannulated with a lacrimal cannula and a syringe containing 5ml of saline. Saline should appear at the lower punctum or at the nares when the lower punctum is occluded by gentle digital pressure. Dacryocystorhinography - 0.1-1.0ml positive contrast used to delineate the nasolacrimal system.

23

What is a congenital imperforate puncta?

Produces epiphora in young animals frmo about 8 weeks of age. the duct system is present but the punctum is occluded by a thin covering of conjunctiva. The diagnosis is made by direct disualisation, confirmed by flushing. The saline will form a bleb at the site of occlusion. The covering membrane can be simply surgically excised.

24

How should lacerations of the nasolacrimal duct be treated?

Acute lacerations should be treated by cannulation of teh caniculis with monofilament nylon, over which a fine polypropylene tube is passed. the cannula should be left in place for 14 days until the wound has healed.

25

What is dacryocystisis?

Inflammation of the lacrimal sac (usually plus inflammation of the duct and canaliculi) most often due to a foreign body such as a grass seed. Flushing of the system from the upper punctum may allow the foreign body to be grasped at the lower punctum. Retrieval from the lacrimal sac is less straightforward but the lacrimal sac can be incised from a conjunctival approach using probes or plastic cannulae to identify site of incision. repeated flushing and systemic and topical antibiotics usually needed to prevent occlusion of the duct.

26

Describe the anatomy of the cornea?

The corneo scleral coat is the outermost fibrous coat o the eye. The cornea is a transparent continuation of the sclera, the junction is termed the limbus. The cornea relies on the aqueous and tear film for nourishment and cleansing and the third eyelid and lids for protection from the external environment. the cornea consists of 5 layers.

27

Describe the 5 layers of the cornea

A) anterior outer epithelium - continuous with the conjunctival epithelium at the limbus. Non keratinised, stratified squamous epithelium with rapid turnover of cells. Basement membrane produced by deepest layer of epithelial cells. Hemidessmosomes attach the basal cells to the thin basement membrane, which in turn anchors the epithelium to the stroma. Connective tissue stroma - 90% of corneal thickness, composed of collagen lamellae, separated by ground substance and fibroblasts. D) Descemets membrane - the basement membrane of the underlying endothelium produced throughout life, elastic and fairly strong, does not stain with fluorescein. Endothelium - the deepest layer, important for maintaining corneal dehydration. The cornea is avascular, deriving its nutrition from the aqueous perilimbal capillaries and the tear film. The corneal reflex is the reflection of the light in the cornea.

28

The normal cornea is transparent. Pacities in the cornea take the form of what?

1)oedema,
2) cells infiltrating the cornea or depposited on the endothelium
3) blood vessels - distinguish superficial vessels from deep vessels (deep are darker red, dont cross limbus, straight like hedges)
4) pigment
5) disorganised collagen
6)lipid

29

What is a corneal dermoid?

A congenital mass of hairy skin on the cornea, usually at the lateral limbus. The hairs on the dermoid can irritate the corneal surface. The mass is removed by superficial keratectomy, incising in clear cornea and following a superficial plane of dissection under the mass.

30

What is pigmentary keratitis?

Pigment may be carried in from the limbus along with new bood vessels in response to a variety of chronic corneal insults damaging the occular surface. It is a sign, not a diagnosis. IT is most frequently seen in brachycephalic breeds, due to prominence of the globe, macropalpebral fissure, nasal folds, medial canthal trichiasis, medial canthal entropion - all of which disrupt the tear film. Also seen in chronic KCS, entroion, pannus etc. Pigment tends to remain permanently though

31

What is chronic superficial keratoconjunctivitis?

A chronic superficial vascular keratitis occuring mostly in german shepherd dogs, less commoonly greyhounds. Atypically rough fleshy looking infiltrate of inflammatory cells, pigment and vessels advances across the cornea from the ventro lateral limbus. the corneal epithelium is intact therefore does not stain with fluorescein and signs of discomfort are mild or absent. There may be concurrent involvement of the third eyelid. visual loss can occur in the worst affected cases.

32

Describe age related corneal endothelial degeneration?

Bilateral but usually asymmetrical, degenerative condition of the corneal endothelium occuring as a senile change in old dogs. the loss of endothelial cells causes faiilure of the endothelial pump mechanism resulting in the steamy blue appearance of stromal oedema. Diffuse oedema can be caused by glaucoma or severe uveitis.

33

What is corneal endothelial dystrophy?

Similar to age related corneal endothelial degeneration but resulting from dystrophic endothelial cells so presenting at an earlier age in affected breeds.

34

What is corneal dystrophy?

Primary, bilateral inherited disorder characterised by well demarcated central or paracentral grey/white crystalline opacities. composed of cholesterol, phospholipids and fatty acids, under magniification show a crystalline, fiibreglass like quality. No pain, no vasculratisation and rarely any effect on vision. Treatment is not necessary.

35

What is corneal degeneration

Occurs when the deposition of lipid is seen in association with inflammation and vascularisation - the location and extent of lipid deposition is variable. The aetiology is complex - lipid may be produced in situ or circulating lipid may enter the cornea. Lesions consist of cholesterol, phospholipids, fatty acids and calcium. Corneal degeneration can improve with further vascularisation and phagocytosis, so avoid topical corticosteroid usage. the condition is not painful if the overlying epithelium is intact. Refer patients with recurrent erosions over the lesion for lamellar keratectomy.

36

What is lipid keratopathy (corneal lipidosis)

Uni or bilateral occular manifestation of systemic disease characterised by peripheral or central crystalline opacities and a clear perilimbal zone. Corneal vascularisation may develop with chronicity. screening for underlying systemic lipid abnormalities is indicated e.g hypothyroidism , pancreatitis, DM, hyperlipoproteinaemia.

37

What is a corneal arcus?

Bilateral peripheral lipid deposition, uncommon, invariably associated with plasma hyperlipoproteinaemia and the underlying cause should be determined.

38

What is corneal ulceration?

The corneal epithelium provides a protective barrier which is resistant to bacterial colonisation and prevents water entering the cornea. Loss of full thickness of the epithelium (most often as a result of mechanical traua) exposes the underlying stroma. Under certain circumstances Successful bacterial colonisation in particular, there may be further Stromal loss and ultimately full thickness corneal perforation.

39

Describe the normal healing of ulcers?

Healing of epithelial defects is usually rapid, achieved by the migration of adjacent basal epithelial cells to cover the defect, which then replicate to restore the full epithelial thickness. superficial ulcers heal within a few days in healthy individuals. The stromal defects of deeper ulcers are initially filled by a fibrin clot. Activated keratocytes at the wound edges secrete collagen, aided by invading fibroblasts. This new collagen tends to be disorganised and a permanent opacity is likely when deeper ulcers heal. Scarring is less in cats than dogs. Stromal healing takes longer than re epithelisation. Full stromal thickness may never be regained, leaving an epithelialised depression, known as a facet.

40

What are the clinical signs of corneal ulceration?

Discomfort - usually marked. Lack of pain indictes abnormal corneal sensatino. Conjucntival hyperaemia, variable amounts of localised corneal oedema and irregularity of the surface contour, neovascularisation and cellular infiltration of the cornea common with chronic ulcers, secondary anterior uveitis, tends to be more apparent in deep ulcers.

41

How is a clinical assessment of a corneal ulcer done?

Apply topical anaesthetic and fluorescein (STT first unless obviously lacrimating or ulcer deep), draw diagrams indicating - surface area, site, depth, edges, (obvious vs. Underrun or gelatinous), look carefully for an underlying cause. identify any factors that may complicate or compromise normal healing including topical steroids which are contra indicated in the presence of corneal ulcers.

42

What are the causes of corneal ulcers?

External trauma, hair/lash trauma (entropion and ectopic cilia), infection (FeHV), bacterial colonisation secondary to trauma, rarely fungal, tear film abnormalities - acute dry eye, exposure keratopathy, SCCED, rupture of epithelial bullae in very oedematous corneas, epithelial erosion by corneal cholesterol or calcium deposits. The site gives important clues as to the likely cause. most ulcers are caused by hit and run type injuries and therefore usually centrally located. The site of ulcers caused by an abnormal hair contact will be determined by the location of the lid abnormality. An ectopic cilium should be suspected when the ulcer is dorsally located. Ulcers under the third eyelid should not be overlooked - check for a foreign body.

43

What is exposure keratopathy?

Refers to the central corneal damage resulting from inadequate protection of the cornea by the eyelids and third eyelid, which may be compounded by inadequacy of the pre ocular tear film. causes are varied and include 1) prominent globe with poor lid closure - brachycephalics, megaglobus of chronic glaucoma, retrobulbar masses. 2) facial nerve paralysis - not usually a problem for breeds that can retract their globes sufficiently to spread the tear film with the third eyelid, brachycephalics struggle to do this. 3) trigeminal nerve paralysis - absent corneal sensation results in a severe keratitis affecting the area of cornea exposed between the lids. Brachycephalics have reduced corneal sensation.

44

Describe the depth of a corneal ulcer

the majority of ulcers are superficial involving little stromal loss. they may not be visible without fluorescien. there is usually more oedema around deeper ulcers and an obvious step down to the ulcer crater. most deep ulcers were superficial initially and should be treated as though they were infected as this is the most likely cause of ulcer progression. If the ulcer extends through the full thickness of the stroma to descemets membrane the cornea is in imminent danger of rupture. suspect a descemetocoele if the centre of the ulcer appears clear. The centre of the ulcer is usually at the base of an obvious depression but in some cases descemets membrane may balloon forwards. Fluorescein staining of a descematocoele produced a green halo of stain with a clear centre as descemets membrane repels the stain.

45

What is the treatment of an uncomplicated superficial ulcer?

Left untreated, most acute superficial ulcers in healthy animals would heal quickly once the cause is no longer present. However as the consequences of infection are serious, topical broad spectrum antibiotics should be applied until the cornea is fluorescein negative. arrange revisit appointment 5-7 days to confirm resolution.

46

What is the treatment of superficial under run ulcers( superficial chronic corneal epithelial defects or SCCED)

Ulcer healing will be severely compromised if the edges of the epithelium fail to adhere to the underlying stroma. this creates a flap or underrun edge at the ulcer margin, w hich may be recognisable on pentorch examination. Apply topical anaesthesia and push back the edge of the ulcer with dry sterile cotton tipped applicators. the loose epithelium wil peel back, enlarging the ulcer, Dry debridement usually followed by a second procedure to augment healing in the dog, including debridement with a diamond burr, superficial grid keratotomy or superficial punctate keratotomy.

47

How can midstromal ulcers be managed?

medically with broad spectrum topical antibiotics every 2-6 hours such as neomycin, bacitracin, polymyxin combination or ciprofloxacin. Treat accompanying reflex uveitis with atropine as needed to idlate the pupil and anti collagenase 3-4x day .

48

How can deep ulcers / descemetocoeles be managed?

high risk of corneal perforation - emergency referral recommended unless you are equipped to perform corneal surgery. Cytology and culture should be performed. The edge of the ulcer is swabbed then gently scraped using the blunt end of a scalpel blade. this is best performed under ssedation or GA to reduce the risk of iatrogenic perforation and is followed by surgery to support the cornea. (conjunctival pedicle graft or corneal conjunctival transposition - not a third eyelid flap) . Some deep and even melting ulcers are sterile but do not assume this. treat empirically with a topical fluoroquinolone (concurrent use of systemic doxycycline has also been recommended for its anti protease activity. Apply fluoroquinolone frequently initially - every 5 minutes for first 30 minutes and then every 1-2 hours. do not use ointments where there is a risk of perforation or when perforation has already occured.

49

What is a melting ulcer?

Enzymatic breakdown of the cornea can accelerate, causing rapid dissolution of the stroma. the enzymes responsible originate from abcteria, PMNS and from the cornea itself. Melting is recognised when the edges of the ulcer appear gelatinous as though they would not be able to hold a suture. Best refer as emergency surgery - debridement of the melting portion and surgical support of the cornea with a pedicle graft is often indicated. In addition to antibiotic therapy, an anti collagenase should be given. Serum 5-10% acetylcysteine or 0.17% ETA. Serum works well in dogs and cats. Allow to clot and centrifuge to obtain serum.

50

What is a conjunctival pedicle graft?

Corneal surgery requires microsurgical instrumentation, magnification and technical expertise. early referral of deep or melting ulcers is encouraged. perforated ulcers can be successfully repaired using specialist techniques if referred early.

51

How should corneal injury be managed?

Specialist advice - lavage is most important initial step and should be instituted immediately. Acid injury - less dangerous than alkali as proteins coagulate to limit penetration. treat with copious lavage with sterile saline, analgesia and then as for corneal ulceration. Alkali - causes corneal melting, severe uveitis, irrigate over several hours, use protease inhibitors and treat uveitis. Detergents/spirit - both will strip the epithelium so use only 0.2% aqueous povidine iodine for preparation of the occular surface.

52

How is corneal laceration managed?

If not penetrating or very deep then treat for ulcerative keratitis. flaps of cornea can be removed to aid healing unless the laceration is deep enough to require suturing. penetrating injury may be self sealing if small. larger injuries seal with iris and coagulated aqueous and are best Reffered as an emergency. Anterior uveitis is invariably present. Poor prognostic findings; penetration of lens capsule - severe uveitis unless lens removed, very large lacerations, extension of laceration into sclera, expulsion of lens or vitreous, severe Intraocular haemorrhage, laceration due to blunt trauma. Treat small wounds - topical antibiotics, atropine, systemic antibiotics and NSAIDS.

53

What is the anterior uvea?

Consists of the iris and ciliary body. The posterior uvea is the choroid and is best considered with retinal disease in the clinical setting. The uvea is the most vascular most pigmented and most immunologically reactive tissue in the eye. The iris - is a diaphragm to control the amount of light entering the eye. the posterior epithelium is densely pigmented but the amount of pigment in the stroma varies determining the eye colour. this is also reflected in the amount of pigment in the choroid and to some extent the hair coat. On close examination the iris may have an irregular surface contour. Pupil size is largely controlled by parasympathetic tone in nerve III. Ciliary body has 3 functions; accomodation, produced by ciliary mm.
Attachment of the zonule supporting the lens via ciliary processes.
3. Active secretion of aqueous by inner non pigmented epithelium.

54

What is persistent pupillary membrane remnants?

Strands of the iris tissue (embryological remannts) running from mid iris to the cornea, where they cause a focal corneal opacity at the point of attachment, the lens where they may cause a capsular subcapsular cataract at the point of attachment, or across the pupil to the iris, sometimes in a web like pattern.

55

What are uveal cysts?

Uveal cysts may arise form the posterior surface of the iris or the ciliary body, usually spontaneously but sometimes following uveitis. they often break free and move around the anterior chamber. they may rupture leaving remnants on the corneal endothelium. Treatment not normally necessary. the main concern being distinguishing them from intraocular melanoma. Iris cysts are spherical and not solid.

56

What is a naevi?

A naevus is a patch of hyper pigmentation which, although it may increase in area, does not protrude beyond the contour of the iris. Observe only. Problematic in the cat as difficult to distinguish from early intraocular melanoma.

57

What is anterior uveal melanoma?

This is the most common intraocular tumour in all species. Usually the appearance is of a heavily pigmented solid mass within the iris or in the ciliary body. they are often unrecognised by the owner until the development of secondary gluacoma. In the dog and horse they generally exhibit benign behaviour and grow slowly and enucleation is usually curative.

58

What is a limbal melanoma?

Heavily pigmented tumours arising at the limbus. they are not uveal tumours but can resemble a tumour invading out through the sclera. they grow slowly, gradually invading the cornea and sclera and do not metastasise. Regional excision is a specialist procedure. GSDS predisposed.

59

What is a ciliary body adenoma?

Presents as a well defined, pink mass protruding into the pupil. The more aggressive ones may invade the iris. The prognosis is generally favourable following enucleation.

60

What are non pigmented limbal masses?

Other non pigmented masses are seen at the limbus and or invading the cornea. they are rare, proliferative inflammatory lesions of unknown cause, classified according to their appearance and extent as episcleritis, nodular episcleritis and nodular episclerokeratitis. Most respond to steroids. Unless there is obvious intraocular involvement, do not remove an eye under suspicion of neoplasia without first confirming the diagnosis.

61

What is anterior uveitis?

Inflammation of the iris and ciliary body is known as anterior uveitis. The pain in acute anterior uveitis can be intense, mainly as a result of ciliary and iris muscle spasm. chronic low grade uveitis is less painful and the owner may be more concerned with the change in appearance of the eye than the discomfort. because of the close anatomical relationship with the retina, inflammation of the posterior uvea occurs in conjunction with retinal inflammation which is not painful unless the anterior uvea is also inflamed presenting instead with visual loss.

62

What are the signs of acute anterior uveitis?

Pain (lacrimation, enopthalmos, blepharospasm, photophobia) visual disturbance, red eye - episcleral and conjunctival hyperaemia/congestion. Circumlimbal prominence of deep episcleral vessels that move with movements of th globe. Corneal oedema - usually only mild due to endothelial dysfunction - very severe in adenovirus infection. Breakdown of the blood aqueous barrier allowing protein and inflammatory cells into the aqueous. (aqeuous flarE). Miosis - constricted pupil which responds poorly to light, swelling of the iris - looks puffy and dull with loss of surface detail. Reduced intraocular pressure - drainage of aquous via the uveoscleral pathway is increased resulting in decreased IOP

63

What are the complications of anterior uveitis & signs of chronic uveitis?

Synechiae formation - when inflamed the iris becomes sticky and may form adhesions to the cornea, (may cause glaucoma) to the lens capsule (distortion of posterior chamber to anterior chamber, causing a pupil block glaucoma - iris bombe).
Glaucoma - several factors - namely extensive synechiae formation, fibro vascular membrane proliferation at the iridocorneal angle and occlusion of the drainage angle with inflammatory cells and debris. 3) iris colour change - typically darening. In Uveodermatological syndrome, the iris loses pigment however.
4) vitreal opacities or floaters - exudation of protein and inflammatory cells from the ciliary body confers a hazy appearance to the anterior vitreous which may later organise. 5) cataract formation and lens luxation 6) pthisis bulbi

64

What are the causes of anterior uveitis?

Local to the eye - corneal injury and ulceration (reflex uveitis), blunt and penetrating trauma, release of antigenic lens protein, intraocular neoplasia.
Associated with systemic diseases 1- Septicaemia/bacteraemia/toxaemia (e.g pyometra, anal sac abscessation, bite wound), 2- Infectious diseases, 3 - lymphoma.
Many cases of canine uveitis the cause remains obscure despite a thorough work up. These are thought to be immune mediated probably due to sensitised immunocompetent cells in the uvea responding to circulating or intra ocular antigens. Most cases respond to symptomatic treatment. A systemic work up is warranted if the inflammation is moderately severe to severe in both eyes, vision is threatened and posterior segment disease or systemic disease is present.

65

What is the therapy for anterior uveitis?

Deal with cause, reduce intraocular inflammation and restore blood aqeous barrier, achieve moderate mydriasis and pain relief, moitor IOP in order to detect any secondary glaucoma, steroids and non steroidal anti inflammatory agents may be used to control inflammation and may be given topically or systemically. Topical corticosteroids should begin immediately if the cornea is intact. choose a preparation with good corneal penetrating ability. Topical NSAIDS may be used if the cornea is ulcerated but may slow corneal epitheliasation and probably contra indicated in severely infected ulcers. Systemic steroids indicated when the inflammation is sever and involves the posteroir segment. Systemic Nsaids are usful when it is unsafe to use systemic steroids or while waiting for diagnostic tests to be performed.

66

What are mydriatics/cycloplegics?

Atropine dilates the pupil, reducing the risk of extensive posterior synechiae formation. IT also relieves pain due to muscle spasm. It is much less effective in an inflamed eye and should therefore be given at frequent intervals in the initial stages, every 2-4 hours aiming for a reasonably dilated pupil. monitor the IOP - atropine is contraindicated if the pressure rises above normal. only exception being early cases of iris bombe.

67

How is aqueous drained from the eye?

Aqueous drainage is produced by the ciliary body, passes through the pupil into the anterior chamber and drains at the iridocorneal angle. There it passes between the strands of the pectinate ligament and flows through the sponge like trabecular meshwork of the ciliary cleft to reach the angular aqueous plexus. From there it drains into the scleral veins and general circulation. A small portion of aqueous outflow occurs via the uveoscleral route, bypassing the trabecular meshwork.

68

What is glaucoma?

Glaucoma is an elevation in intraocular pressure incompatible with normal function of the eye. it is an important cause of pain and visual loss in the dog, less common in the cat. it arises when outflow of aqueous is compromised by mechanical obstruction or functional failure of the irido-corneal drainage angle. it may also occur if the passage of aqueous through the pupil is blocked. Clinical signs vary according to rate, duration and severity of increase in IOP.

69

What are the signs of acute glaucoma in the dog?

1) Pain: can be severe, with lethargy and avoidance behaviour
2). visual loss: as glaucoma usually presents unilaterally this may go unnoticed
3) episcleral congestion - sinuous, engorged blood vessels running perpendicular to the limbus which do not move with the conjunctiva
4) corneal oedema resulting in a steamy appearance 5)moderately dilated pupil, poorly responsive to light
6) elevated IOP. glaucoma confirmed by tonometry. IOP measurement should be performed in every patient with unexplained red eye, Occular pain or visual loss. Elevated IOP Can result in irreversible damage to the optic nerve and retina within a matter of hours. Acute glaucoma is a neurological emergency with a narrow window of opportunity for successful treatment.

70

What are the signs of chronic glaucoma?

Signs can occur rom previous bouts of acute glaucoma or wiht an insidious rise in IOP.
1) Buphthalmos, megagloblus, globe enlargement. 2) Variable corneal vascularisation and pigmentation may get deep corneal vascularisation. 3) lens subluxation/luxation due to rupture of the zonule as the globe enlarges, tears in descemets membrane, seen as grey/white streaks due to stretching of the cornea. Visible retinal degeneration and optic disc cupping. Variable degree of pain.

71

What is primary glaucoma?

Generally seen in predisposed breeds. the developmental abnormality is bilateral although one eye tends to decompensate before the other so it presents uniltaerally. does not occur til middle age. Poor long term prognosis for vision and comfort. Primary angle closure glaucoma is most common form. Drainage angle of contralateral eye will be seen to be abnormal. decompensation of predisposed eye occurs within 2 years - freq 6 months.

72

What can cause secondary glaucoma?

Primary lens luxation, uveitis, intraocular neoplasia, intraocular haemorrhage, retinal detachment, pigmentary glaucoma of the cairn terrier, in most instances the above are readily recognisable on occular eamination. If corneal or lens opacities or Intraocular haemorrhage prevent adequate direct visualisation Occular ultrasonogrpahy is indicated to detect intraocular neoplasia or retinal detachment.

73

How is glaucoma managed?

Genuine emergency - sustained high IOP will cause collapse of the ciliary lefft and formation of anterior synechiae, preventing any future successful outcome. management may be medical /surgical. First decide whether problem is primary or secondary. attend to cause of secondary glaucoma wherever possible.

74

What are occular hypotensive agents?

Prostaglandin analogues - potent topical occular hypotensives causes pronounced miosis should be avoided in gluacoma secondary to uveitis and anterior lens luxation. Used to treat primary glaucoma.
Osmotic diuretics - in emergency. most often in treatment of acute primary glaucoma. Contract vitreous and will keep the IOP down for several hours.
Carbonic anhydrase inhibitors - reduce aqueous production b up to 40% by reducing the amount produced by active secretion. Acetalozamide or brinzolamide or dorzolamide.
B blockers - small reduction in aqueous production by reducing blood flow through the ciliary processes e.g topical 0.5% timolol, betaxolol.
cosopt is a combination of dorzolamide and timolol develop for twice daily topical use.

75

What are the guidelines for management of glaucoma depending on underlying cause?

1. Suspected primary angle glaucoma - seek specialist, PG analogue, CAI
2) primary lens Luxation - CAI, topical steroids, refer for lendectomy
3) anterior uveitis: topical and systemic corticosteroids, plus CAI, do not use PG analogue or mannitol - atropine contraindicated
4) Intraocular neoplasia: enucleation curative in most primay tumours
5) Intraocular haemorrhage - address source of haemorrhage, CAI
6) retinal detachment - enucleation as there is no prognosis for vision
7 pigmentary glaucoma of cairn terrier: seek specialist Advice, PG analogue, CAI.

76

What is the surgical treatment of glaucoma?

Long term success frequently disappointing. All require specialist equipment, specialist experience and money. endoscopic cyclophotocoagulaion - laser of the ciliary processes is currently the most promising development but requires lens removal to be most effective.

77

Describe the anatomy of the lens

The lens is transparent and avascular receieving its nutrtitional requirements via the aqueous. it is made up of lens fibrees enclosed within an elastic capsule. the capsule prevents exposure of lens fibres to the foetal circulation during the period when immune tolerance develops - lens fibres therefore remain antigenic throughout life and cause uveitis if the capsule is breached. The lens fibres meet at suture lines to form an upright Y anteriorly an inverted Y posteriorly. the lens is suspended by zonular fibres fomr the ciliary body which attach at the lens equator. in the dog the lens is relatively firmly attached to the anterior face of the vitreous. the anterior epithelium of the lens continues to divide throughout life. the cells are pushed towards the equator where they elongate and lose their nuclei to form secondary lens fibres surrounding the nucleus.

78

How is the lens examined?

Using a simple light source and some magnification, although mydriasis is often essential. Distant direct opthalmoscopy is a simple technique demonstrating even small opacities effectively and is a quick way to assess the overall clarity of the lens.

79

What is nuclear sclerosis?

A normal ageing change, gradually becoming apparent frmo about 6 years onwards. As more secondary lens fibres are laid down, condensation and compression of the nucleus occurs, imparting a blue grey appearance to the nucleus frequently mistaken for a cataract by the owner. It has no effect on vision. It can be distinguished readily from a cataract as it does not appear as an opacity in distant direct opthalmoscopy. A faint refractile ring may be seen around the nucleus when the pupil is dilated.

80

What is primary lens luxation?

The most common cause of lens Luxation in the dog. Primary lens luxation typically seen in terrier breeds with proven inheritance in some breeds. A DNA test to determine a dogs genotype with respect to PLL has been developed, testing kits available. there is a primary abnormality of the zonule, leading to subluxation initially followed by Luxation as the last of the zonule breaks down. Usual scenario is a dog between 2-5 years of age presenting with a luxation in one eye and subluxation in the other. Including iriododenesis, a wobble like oscillation due to lack of iris support by the lens. the iris appears flat and the anterior chamber deeper than normal for the same reason. An aphakic crescent may be seen dorsally. This represents a crescent shaped gap between the lens equator and the iris which is most obvious if the pupil is dilated. When the lens is free to move within the eye, the last of the zonule has broken down it may move either anteriorly into the anterior chamber or posteriorly into the vitreous.

81

Dscribe anterior lens luxation

Causes acute glaucoma, the lens and vitreous physically obstructing the flow of aqueous through the pupil. The usual presentation is one of an acutely uncomfortable red eye. vision will be impaired in the affected eye. the lens will come into contact with the endothelium of the cornea, causing a local sub central corneal opacity.

82

What are the signs of posterior lens luxation?

Similar to those for subluxation although the aphakic cresent may dissapear if the lens falls right back into the vitreous. 90% of lenses will luxate forward into the anterior chamber at some oint and may cause glaucoma.

83

What is the treatment for lens luxation?

An anterior luxated lens needs to be surgicalyl removed as a matter of urgency as glaucoma cannot be controlled with medical treatment. Intraocular surgery is a specialist techniqe. Arrange refferal. subluxated lenses may be anaged medically with prostaglandin analogues to keep the lens behind the constricted pupil and maintain a low IOP or surgically by elective lendectomy using phacoemulsification. posterior lens Luxation does not usually cause acute problems and the lens may be left in the vitreous with judicious use of a prostaglandin analogue but the owners should be made fully aware of the signs to look for if the lens moves forwards.

84

What is a cataract?

Any opacification - focal, partial or total of the lens or its capule. Disruption of fibre arrangement, accumulation of insoluble proteins and oedema due to the accumulation of osmotically active substances may all be involved in the pathogenesis.

85

What is secondary lens l uxation?

May occur secondary to chronic glaucoma (enlargement of the globe stretches then ruptures the zonules), chronic anterior uveitis (uncommon in dogs - seen mostly in cats), severe occular trauma, hypermature inflexible cataracts. The management is determined by the cause - lendectomy may be appropriate if there remains the potential for a comfortable and visual eye. enucleated indicated in chronic glaucoma.

86

How may cataracts be classified by their site?

Describe the position and extent of the opacity within the lens using the accepted terms e.g nuclear, cortical, polar, equatorial, capsular or subcapsular. this allows monitoring for progression and allows the cataract to be compared with known forms of inherited cataracts in that particular breed.

87

What are incipient cataracts?

The earliest stage with small opacities or vacuoles affecting <15% of the lens. not all are progressive. no obvious effect on vision.

88

What are immature cataracts -

more extensive opacities, but a fundic reflex still present. Vision variably affected , depending on extent and position of opacities.

89

What are mature cataracts?

Total opacity with no fundic reflex, causing blindness.

90

What are hypermature cataracts?

The lens contracts giving an irregular wrinkled surface especially when viewed obliquely and a deep anterior chamber. it ma leak protein leading to a low grade uveitis or become so inflexible that zonular fibres rupture.

91

What are morgagnian cataracts?

Resorption and clearing of cataractuous cortex may occur in some cataracts. the cortex liquifies and may take on a metallic glistening appearance before resorption but uveitis is a risk at this stage. the nucleus remains solid and may sink to the bottom of the lens.

92

What is an intumescent cataract?

Very rapidly developing cataract e.g in diabetes mellitus, which may swell sufficiently to cause a shallow anterior chamber and even obstruct drainage and or leak lens protein leading to uveitis.

93

Describe congenital cataracts.

Most congenital cataracts are not hereditary but caused by some distrubance in utero. they may be associated with other occular defects e.g micropthalmos. they tend to be nuclear cataracts and be non progressive and as more secondary lens fibres are laid down around the nucleaus they become relatively smaller and vision may improve. topical atropine can be used 1-2weekly to improve peripheral vision around a nuclear cataract.

94

Describe hereditary cataracts?

most develop in first few months or years of life. any will lead to blindness. commonly encountered is the posterior polar sub-capsular cataract seen at the confluence of the suture lines. this is only rarely progressive and in the great majority of affected dogs causes on obvious visual impairment.

95

What are diabetic cataracts?

Cataracts associated with diabetes mellitus are usually bilateral and rapidly progressive sometimes leading to blindness within days. this may be first sign of the disease. typically teh cataract is total and diffuse with clearer zones along the suture lines. the accumulation of osmotically active sorbitol within the lens causes water logging. diabetic patients can be good candidates for cataract surgery and cataract surgeons are accustomed to managing their particular requirements. Aldose reductase inhibitors may play a role in delaying the onset or slowing progression of diabetic cataracts in dogs.

96

What are cataracts secondary to ocular disease?

Most importantly gPRA (especially in miniature and toy poodles, english cocker spaniels and labradors). These cataracts arise secondary to the retinal degeneration and generally progress to maturity. Removal of these cataracts will not prevent blindness. Cataracts may also arise secondary to glaucoma (changes in aqueous composition and damage to anterior lens epithelium), retinal dysplasia and RPEd. Uveitis causes secondary cataract formation in cats and horses but this is rare in the dog.

97

What are senile/spontaneous/idiopathic cataracts?

Common in the dog. N -acetyl carnosine may reduce the rate of progression and reduce the extent of the opacity if given to these dogs with early lens changes,but has no effect on lens clarity in mature cataract.

98

How are cataracts managed?

Cataract surgery is most definitely a specialist procedure only. Hypermature cataracts are associated with a worse outcome and surgery should not be unduly delayed.

99

What is the vitreous?

The vitreous is a soft gel comprising 90% water, with some collagen and hyaluronic acid, it fills the posterior part of the eye, conforming to the shape of the surrounding structures. It is quite firmly attached to the posterior lens capsule and plays an important role in retaining the retina in position.

100

What is persistent embryonic vasculature?

the hyaloid artery and hyperplastic posterior vascular tunic of the lens may persist indefinitely appearing as a fibrovascular plaque immediately behind the lens along with a posterior capsular cataract. Treatment is not usually attempted. It is inherited i n the SBT and doberman. As an incidental finding of no clinical signficance, the hyalod artery can remain as a worm like projection from the optic disc or the back of the lens into the vitreous.

101

What is vitreal syneresis?

Liquefaction of the vitreous occurs as an irreversible degenerative change secondary to glaucoma, lens luxation, uveitis or senility. It predisposes the eye to retinal detachment, as liquified vitreous can peroclate beneath any holes in the neurosensory retina.

102

What is asteroid hyalosis?

Numerous minute opaque spheres of a clacium/lipid complex suspended throughout the vitreous are not uncommonly seen in older dogs. They may be unilateral. The pathogenesis is obscure, the eye is sometimes otherwise normal, but they can also be associated with other intraocular disease (neoplas,a retinal degeneration) or systemic hypertension.

103

What are vitreal opacities?

Vitreal floaters are sometimes seen as an incidental finding or they may be condensed exudate from previous posterior segment inflammation. Exudate or haemorrhage attached to the retina can cause traction, detaching the retina as it contracts. In active posterior segment inflammation they may be vitreal haze due to the presence of inflammatory cells in the vitreous. This can interfere with the view of the fundus, it appears out of focus.

104

Describe the orbit

The orbit contains the eye, optic nerve, lacrimal and nictitans gland, extraocular muscles, blood vessels and nerves in a cone shape. The zygomatic salivary gland lies at the floor of the orbit rostrally. The orbital ligament spans the gap between the zygomatic process of the frontal bone and the frontal process of the zygomatic bone. It can be palpated as a taut band, the lacrimal gland lies beneath it. The medial bony wall of the orbit separates it from the nasal cavity - the bone here is thin and easily breached by nasal tumours. The close proximity of the masticatory muscles, the frontal and maxillary sinuses, caudal molar tooth roots, caudal nasal chamber, pharynx and zygomatic gland mean that disease in these structures may extend nto or distort the orbit and its contents.

105

What are the clinical signs of orbital disease?

May include a combination of the following, not all of which are specific for orbital disease;
Exopthalmos - protrusion of the globe
Difficulty in digital retropulsion of the globe
Third eyelid protrusion
Pain on opening the mouth (especially with retrobulbar cellulitis/abscess/myositis)
Conjucntival hyperaemia/chemosis/congestion
Deviation of the globe (strbismus)
Lagopthalmos and exposure keratopathy
enopthalmos: rare - due to destruction/ loss of orbital contents
Orbital swelling
Unilateral problems are most comoon, bilateral involvement would suggest myositis.

106

What are the DDx for orbital disease?

Retrobulbar tumour, retrobulbar cellulitls/retrobulbar abscess

Masticatory or extraocular myositis, adenitis of the zygomatic salivary gland, retrobulbar foreign body, retrobulbar haemorrhage, space occupying lesions of the Nictitans gland or zygomatic salivary gland.

107

What is the cause and clinical signs of retrobular abscess/cellulitis?

Orbital infection may be caused by penetration of the skin, conjunctiva or oropharynx with or without a foreign body. IT is rare to find the cause in most cases. Stick/bone chewers most prone. The clinical signs are typically of acute onset, with pain on opening the mouth, exopthalmos, periorbital swelling and often marked conjunctival hyperaemia, the dog may well be off colour - generally lethargy, anorexia and pyrexia may be present.

108

How should retrobulbar abscess be investigated?

Ultrasonography is the most helpful imaging modality. If a focal mass or foreign body is not seen, empirical therapy with broad spectrum antibiotics and NSAIDS will generally result in rapid improvement. Surgical drainage under GA may be of benefit. A swab for bacterial culture should be obtained from the wound, taking care not to contact the oral mucosa. With abscessation, puncture of the abscess cavity releases a free flow of pus. The prognosis is excellent with rapid improvement on antibiotics. If condition recurs on completing the course a foreign body may be implicated.

109

Describe retrobulbar neoplasias

Primary, secondary and tumours arising from adjacent structures. Signs usually develop gradually, with progressive exopthalmos and frequently with deviation of the globe. There is usually little pain on opening the mouth. As many retrobulbar tumours originate from the nasal cavity, check for reduced air flow through the nostril of the affected side.

110

How will retrobulbar neoplasia's appear on imaging

Plain film radiography is a useful technique as it may demonstrate extension from the nasal cavity or loss of orbital bone - both are poor prognostic indicators. thoracic radiographs should also be performed to look for metastases although these are uncommon. Most tumours appear variably hyperechoic on ultrasound and fine needle aspirates may be rewarding, although absence of neoplastic cells on aspirate does not rule out a tumour. CT or MRI demonstrate the extent of the neoplasia most fully and should be considered where available.

111

What s the treatment for retrobulbar neoplasia?

Exenteration - removed along with the eye as an extended enucleation it may be necessary to section the orbital ligament to improve exposure. Excision sparing the globe - refer for orbitotomy: it is however rare to be ale to remove an orbital tumour and retain a functional eye.

112

What is masticatory myositis?

A rare idiopathic inflammatory condition of the masseter, temporal and pterygoid muscles, characterised by infiltration with lymphocytes and eosinophils. In acute masticatory myositis there is bilateral exopthalmos, third eyelid protrusion, pain on opening the mouth and swelling of the muscles, treat with systemic steroids. The chronic form is usually bilateral although unilateral cases exist. Atrophy of the muscles leads to enopthalmos, third eyelid protrusion and mechanical restriction to opening the mouth.

113

What is extraocular polymyositis?

Uncommon condition typically affecting young golden retrievers, causing a bilateral non painful Exopthalmos with reduced ocular movement. Swollen extraocular muscles are seen on ultrasound, CT, or MRI. Treatment with systemic corticosteroids or azathiprine is required to avoid post inflammatory contracture.

114

What is enopthalmos?

Sinking of the eye into orbit will cause a secondary third eyelid protrusion. It is characteristic in dobermans, rough collies, GT danes and FC retrievers, which small eyes and long noses. Mucus may accumulate at the medial canthus but is no cause for concern. Occular pain will cause contraction of the retractor bulbi muscle and globe retraction. Atrophy of orbital tissue - cachexia, severe dehydration and chronic masticatory myositis allow the globe to sink further into the orbit. Horners syndrome - functional denervation of the sympathetic supply to the eye and orbit.

115

What is the fundus?

The fundus refers to the structures at the back of the eye that are visible with an opthalmoscope. Examination may be performed either with a direct opthalmoscope which gives a highly magnified view but a limited field or an indirect opthalmoscope. Assess 4 features - the optic disc, retinal vessels, non tapetal fundus and tapetal fundus. the neuroretina and the retinal pigment epithelium share a common origin from the neural ectoderm developing as the optic vesicle. this invaginates to form the optic cup, the neuroretina forming the inner layer, the RPE the outer layer. The RPE remains a moonolayer whilst the neuroretina differentiates into what might be simplified into a 3 layer wiring system.

116

Describe the path light takes in the fundus

Light has to pass through the transparent cornea, aqueous humour, lens and vitreous before reaching the retina, it must then pass through the glanglion cell layer which contains the retinal blood vessels and the bipolar cell layer of the retina before it finally reaches the photoreceptors (rods and cones).

117

What is the optic disc?

To maintain their transparency, the axons of the ganglion cells are unmyelinate, acquiring myelin as they converge to form the optic disc. The extent of myelination is variable in different dogs and in some breeds may extend some distance beyond the disc margins e.g golden retrievers.

118

Describe the retinal arteries and veins

The retinal vessels enter and leave the retina around the optic disc and travel along side the axons of the ganglion cells. The venules are larger than the arterioles in the dog and may be seen to anastomose over the surface of the disc. These superficial vessels supply the inner layers. the outer layers are supplied by the chorocapillaris, a capillary network just beneath the RPE which is not seen.

119

What is the tapetal fundus?

The tapetum occupies a roughly triangular area dorsal to the disc in dogs. The extent is variable, extending to or below the disc in some dogs, and terminating well above the disc in others. The tapetum is found within the choroid, acting as a mirror to reflect light back to the photoreceptors in dim light. In order for light to reach the tapetum, the cells of the RPE superficial to it are non pigmented. it is not unusual to see islands of pigment in the tapetal fundus close to the border ofthese areas. Long haired dogs tend to have a more irregular junction. In some sub albinotic dogs the tapetumm is very underdeveloped, may only be present as islets. The tapetal area is usually a pale fawn colour in these dogs. The tapetum is not fully develoepd at birth taking about 12 weeks to acquire its adult colour.

120

What is the non tapetal fundus?

Where the fundus lacks a tapetum, it makes sense that light be absorbed as soon as it passes beyond the photoreceptor layer. the RPE is therefore densely pigmented in the majority of animals in this area. the retinal vessels are more difficult to see in the NTF but can be made out against this brown background.

121

What is tapetal hyperreflectivity?

If the retina is atrophic, it becomes thinner. this presents less of a barrier to light reaching and returning from the tapetum. the tapetum will therefore appear brighter (hyperreflective).

122

What is acquired pigment in the tapetal fundus?

Melanocyte activity with pigment deposition may follow a range of insults, including inflammation. Lipofuscin accumulation occurs specifically in retinal pigment epithelial dystrophy and is paler than melanin.

123

What is vascular attenuation?

This occurs secondary to retinal degeneration. the vessels gradually disappearing over time. on early cases this is easist to see in the peripheral fundus and in the finger arterioles around the disc. the larger venules last longest.

124

How does haemorrhage in the fundus appear?

Subretinal haemorrhage appears as small dark spots. Superficial retinal haemorrhage is streaky and radial as it follows the nerve fibre layer and appears assocated with the retinal vessels. Pre retinal (i.e intra vitreal) haemorrhage settles under gravity, assuming a keel shape.

125

What is retinal detachment?

The neuroretina is firmly attached at the optic disc and at the ora ciliaris (around the equator where the neuroretina terminates and becomes the ciliary epithelium). elsewhere, the attachments to the RPE are weaker and may separate. this varies in extent from small focal detachments to 30 degree bullous detachment. the latter is pentorch diagnosis - the retina bulges forward int he vitreous as grey curtains containing the retinal vessels.

126

Describe hereditary retinal disease

the BVA, kennel club and international sheepdog society operate a scheme for certifying pedigree dogs as free of hereditary eye disease. The opthalmic examinations being performed by a panel of opthamologists. The two most likely conditions to be encountered are collie eye anomaly and generalised progressive retinal atrophy. (gPRA).

127

What is collie eye anomaly?

this is a congenital abnormality in which defects of the choroid, optic disc, retina and sclera may arise through impaired mesodermal differentiation. Affects all collie types. inherited as a recessive autosomal trait so there are many carriers. the incidence in border collies is very much lower. The essential lesion is choroidal hypoplasia lateral to the optic disc around the junction of tapetal and non tapetal regions. the pigment in the RPE and choroid is depleted, exposing the whiteness of the sclera between the choroidal vessels in a pale patch. The choroidal vessels appear abnormal in the pale patch. About 30% of dogs also have an optic disc coloboma - varying from shallow depressions in the disc to deep pits extending several millimetres into the optic nerve. total retinal detachment causes blindness in some dogs with CEA, this usually occurs early in life. a number of cases will also sffer intraocular haemorrhage. A number of cases will also suffer intraoccular haemorrhage.

128

What are retinal dysplasias?

RD is a collective term used to describe a number of conditions arising from defective retinal differentiation during occular development. two forms of hereditary RD are recognised. Total retinal dysplasias - pups are born blind with total retinal detachment, sometimes in association with micropthalmia and cataracts. only likely to be seen in lab and english springer.
Multifocal retinal dysplasias - more common - affects several breeds with a pleomorphic clinical appearance varying from a few retinal folds to larrger areas of hyperreflectivity and pigment in the area above the disc. usually no effect on vision, although in the springer spaniel gradual rogressive may occur.

129

What is generalised progressive retinal atrophy?

The primary lesion affects the photoreceptors. These can be classified as photoreceptor dysplasias (histological changes occuring in photoreceptors before they mature at 6 weeks of age) and photoreceptor degenerations ( occur after retinal maturatiion. typical history of gPRA - night blindness, altered granularity or colour of the peripheral tapetal fundus which often striate or radial in appearance and early retinal vascular attenuation. rods Affected first and cones succumb so progresses to total blindness. Tapetal hyper-reflectivity and vascular attenuation more extensive and pronounced and optic disc may look pale or grey. Affected breeds - min and toy poodle, english cocker spaniel, lab retriever, usually develop signs of disease in middle age and develop secondary cataracts.

130

What is retinal pigment epithelial dystrophy?

A rare condition with genetic basis related to reduced ability to utilise dietary vitamin E, most freq recognised in cocker spaniels the fundoscopic changes consist of pale brown spots within the tapetal fundus which represent focal accumulations of lipofuscin. visual loss is slowly progressive. A full neurological examination should also be performed. Proprioceptive deficits being common. dietary supplementation with Vit E can prevent progression.

131

What is sudden acquired retinal degeneration

A condition of unknown aetiology, affect mature adult dogs, dachshunds predisposed, retinal insult leads to apoptosis of the photoreceptors leading to a triad of findings - sudden visual loss, normal fundic exmaination, non recordable electroretinogram. blindness may be preceded by pu,pd, polyphagia, weight gain. over months signs of retinal degeneration will ccur. common to find mild elevations in liver enzymes and cholesterol and although cortisol testing is usually negative for cushings there may be evidence of increased adrenal function. Assessing the pupillary and dazzle light reflexes using red and blue light of specific wavelengths, PLR and dazzle reflexes may persist when the blue light is used in SARd patients ( no response to either red or blue in optic neuritis). - explained by the presence of Melanopsin - a photopigment found in some retinal ganglion cells.

132

What are inflammatory retinopathies?

Inflammation affecting the retina and choroid usually involve both structures concurrently. the underlying cause often goes undetermined but it is important i n active cases to perform a thorough systemic examination with appropriate diagnostic tests. Distemper and toxoplasmosis known causes in the uk.

133

What is active chorioretinitis?

Inflammatory cells accumulating around blood vessels appear as distinct grey/white opacities. thickening of the oedematous retina causes focal hyporeflectivity and haemorrhage and retinal detachment may be present. The vitreous is often hazy.

134

What is inactive chorioretinitis (post inflammatory changes)

With time the affected areas of retina atrophy, leaving focal often sharply demarcated areas of tapetal hyperreflectivity. within the centre of these patches there are frequently dense deposits of pigment. in the non tapetal fundus the areas of damage appear as depigmented irregular patches. although both eyes may be well affected they unlikely will show symmetrical changes.

135

What may cause retinal haemorrhage?

Hypertension, coagulopathies, retinal detachment, trauma, septicaemia, hyperviscosity syndrome eg plasma cell myeloma or leukaemia.

136

what may cause retinal detachment?

Hypertension, chorioretinitis, trauma, CEA, retinal dysplasia. loss of vitreous support, vitreal traction bands, idiopathic/immune mediated. Most detachments are bullous in nature i.e the retina remaining attached at the ora ciliaris and fluid accumulating between the neuroretina and the RPE. the extent of bullous detachment is variable from small focal detachments to extensive separation leading to blindness. secondary glaucoma may occur. Rhegmatogenous detachmetns are less common than bullous detachments. when total rhegmatogenous detachment occurs, the retina is seen to hang limply down from the optic disc and there are no vessels overlying the tapetum. Idiopathic bullous detachment is frequently bilateral and is traditionally treated with prednisolone.

137

What are the effects of ivermectin toxicity?

Excessive dose or use in a susceptible animal (mutation in MDR -1 gene) may give rise to occular signs of mydriasis, blindness, reduced or absent PLR, retinal folds or retinal oedema. often temporary.

138

What is optic nerve hypoplasia?

A rare congenital Hypoplasia of the optic nerve which may be bilateral or unilateral. the disc appears small and greyish in appearance due to lack of myelinated fibres. blindness if severe.

139

What is a coloboma?

A coloboma is any congenital non progressive discontinuity in the occular tissues. The optic disc is affected most often and most of these are CEA related. blood vessels may be seen to tip over the edge of th depression in the disc and disappear. the effect on vision related to the size of the coloboma - many have no obvious effect.

140

What s optic atrophy??

Most often result of advanced retinal degeneration in which other fundoscopic abnormalities will be obvious. these include tapetal hyperrelectivity, retinal vascular attenuation and patchy depigmentation of the non tapetal fundus. the disc appears either dark or pale, flat and small.

141

What is papilloedema?

Oedematous swelling of the optic disc most often occurs as a result of pressure on the nerve within the orbit e.g by a retrobulbar tumour. in human patients papilloedema is a common and reliable indicator of raised intracranial pressure - not the case in the dog. Papilloedema by itself has no effect on vision or the pupillary light responses. the disc protrudes forward so it is out of focus relative to the fundus, focussing on the disc surface using the direct ophthalmoscope requires a more positive setting. the vessels appear to climb up onto the disc surface.

142

What is optic neuritis?

Inflammation of the optic nerve has many causes including infectious agents - distemer, toxoplasma, toxins, granulomatous meningoencephalitis and trauma. these can be expensive cases to work up fully. many are idiopathic. it may appear similar to papilloedema, although the disc margins are less distinct and the disc may look pinker than normal. small haemorrhages near the disc, retinal odema and Vitreal haze may accompany signs. Some cases are retrobulbar, affecting the nerve further back in the orbit - in these cases the fundus appears normal. most present bilaterally and are suddenly blind, the main differential being SARD. swelling of optic nerve may be visible on ultrasound or MRI. Treatment with high doses of systemic steroids is frequently effective in the short term but relapses are not uncommon.

143

Describe the feline eyelids

Conformational eyelid problems are much less common than in the dog although cicatricial entropion can arise as a result of chronic ocular surface pain. cachexia with loss of retrobulbar fat may also cause entropion - temporary relief can be provided with vertical mattress sutures until the cause of the weight loss is determined. congenital agenesis of the lateral upper lid is a rare lesion causing exposure keratitis. eyelid tumours are uncommon but are generally less benign than in the dog - consider referral. SCC in white cats appear as a hairless pink and ulcerative mass.

144

Describe the feline lacrimal system

50% of normal cats will fail the fluorescein drainage test so unless there is asymemtry it can be difficult to be sure of a drainage problem by this means. Cannulation of the upper punctum is best performed under GA in the cat. most persian cats suffer from epiphora due to deformity of the nasolacrimal system and globe prominence - client education necessary rather than treatment.

145

Describe the feline nictitating membrane.

bilateral prominence of the third eyelid is a common sign in the cat, frequently observed in association with systemic disease, particualrly diarrhoea, self limiting but clinical course may last 6-8 weeks. unilateral prominence may be a sign of ocular surface pain, retrobulbar swellings, horners syndrome or symblepharon. lymphoma may involve one or both third eyelids, other tumours are rare.

146

Describe the feline conjunctiva

Conjunctivitis is a common and important clinical condition in the cat. definitive diagnosis of the causative agent can be difficult and empirical treatment is frequently used. the two most important proven causes are feline herpes virus and chlamadophila felis.

147

Describe chlamydophila felis

It is an obligate intracellular bacterium, primary causes conjunctivitis, without respiratory infection, in all ages of cats. it does not cause corneal ulceration. diagnosis iin the acute stage is confirmed by identifying intracytoplasmic inclusion bodies in epithelial cells from conjunctival scrapings. culture of the organism, IFAT or PCR may be performed from swabs or cytology from ventral conjunctival sac. systemic treatment with doxycycilne most effective although topical tetracyclines can be used in cats that will not tolerate systemic treatment. Clavulanic acid potentiated amoxycillin is safe to use in pregnant queens.

148

What is feline herpes virus?

FHV is a frequent cause of conjunctivitis and ulceration not necessarily together. less frequently it presents as stromal keratitis neonatal infection - opthalmia neonatorum. young cats - cat flu with conjunctivitis and sometimes corneal ulceration. older cats - recrudescence of latent infection causing refractory ulcers, stromal keratitis or chronic conjunctivitis. Diagnosis and treatment problematic. Dendritic ulcers pathognomic for FHV. Treatment - general nursing care, broad spec antibiotics, anti viral agents, oral faciclovir/ topical trifluridine in some case. Underrun ulcers should be dry debrided and superficial keratectomy may be of some value. supplementation of diet with Llysine may be useful.

149

What are symblepharon?

Feline conjunctival surfaces tend to form adhesions when inflamed and these may involve the palpebral and bulbar conjunctiva, the nictitating membrane and the cornea in various combinations. it is particularly associated with FHV infections in young cats. sometimes the corneal epithelium is replaced by a conjunctiva like membrane following extensive ulceration. surgery can be attempted but is not straightforward.

150

What is corneal sequestrum?

Only seen in the cat, persians predisposed. clinical signs depend on the stage of disease, appearance is unmistakeable, black plaque extruding through the corneal epithelium and causing pain. best treated by keratectomy. a conjundctival pedicle graft may be useful in preventing recurrence. sometimes no obvious discomfort. the lesion appearing as a tan coloured stromal discolouration - should be monitored as tendency to extrude through epithelium eventually. phenol cautery has been suggested as a possible cause of these lesions.

151

What is eosinophilic keratitis?

Proliferative superficial keratitis of unknown aetiology (infiltrate of lymphocytes, eosinophils, plasmocytes, which typically has a cottage cheese appearance on the cornea near the medial or lateral llimbus, frequently involving the adjacent conjunctiva, it is non ulcerative causing mild signs of occular discomfort but looks alarmingly like a tumour. may be uni or bilateral. diagnosis based on appearnce, corneal scrapings revealing the presence of eosinophils. most respond well to topical steroids, frequently initially then reducing to maintenance levels. topical cyclosporine also effective.

152

What is anterior uveitis?

Frequently associated with systemic disease, particularly FIV, FIP, FeLV and toxoplasmosis. Ocular signs are numerous and include ciliary flush, nictitans protrusion, aqueous flare and fibrin, hypopyon, mutton fat keratitic precipitates, iridial hyperaemia, iridial nodules, decreased intraocular pressure, cellular infiltrates in the anterior vitreous and variable posterior segment involvement.

153

Name the important causes of uveitis in the cat

FIV - low grade chronic uvieitis.
FeLV - malignant cells may infiltrate uvea with obvious iris thickening
FIP - tends to cause a pyogranulomatous uveitis - diagnosis difficult
Toxoplasmosis - posterior segment disease granulomatous chorioretinitis and retinal vasculitis. anterior uveitis may also be present. diagnosis difficult. idiopathic - low grade chronic uveitis in older cats, frequently unilateral. Treatment is symptomatic, topical and ocasionally systemic corticosteroids with mydriasis being provided preferably by atropine ointment rather than drops.

154

Describe uveal neoplasias

Primary and secondary tumours occur in cats, generally carrying less favorable prognosis than dogs. melanomas rae most common. most arise form the iris (rather than ciliary body as in dog) sometimes cause a patchy incraese in pigmentation, difficult to distinguish from benign changes-enulceate if causing secondary glaucoma if there is obvious iris thickening. metastasis to liver and lungs are not uncommon. lymphoma also occurs within the eye. primary intraocular sarcomas may occasionally appear years after trauma or chronic inflammation in the eye. trauamtised blind eyes in the cat should be checked periodically if left in situ as sarcomas are malignant in behaviour. intravitreal genticin should never be used in the cat.

155

What is glaucoma?

normal IOP in the cat is 20.2 +/- 5.5mmHg. readings over 32 with the schiotz are significantly elevated. onset of clinical signs in cats often insidious, they may only show mydriasis with less episcleral congestion or overt discomfort than the dog. most glaucoma in the cat is secondary to obstruction of the drainage angle from chronic or acute uveitis. prostaglandin analogues do not lower IOP in this species. Cosopt is widely used (dorzolamide and timolol)

156

Describe the feline lens?

Primary and diabetic cataracts and primary lens luxation are not important int his species. uveitis is the most common cause of cataract formation, it may also cause lens luxation. penetrating injury involving the lens may also lead to uveitis and cataract formation. cataract removal is feasible, the underlying uveitis must also be addressed.

157

Describe the feline fundus?

There is much less variation int he normal feline fundus compared to the dog. the tapetum is very bright, most frequently a yellow green colour. the disc is usually found 1-2 disc diameters in the tapetum, it is round dark grey pink and the vessels do not anastomose on the disc surface. the ganglion cell axons myelinate at the level of the lamina cribrosa in the cat not around the disc as in the dog. papilloedema is therefore more difficult to recognise. the fundus immediately adjacent to the disc frequently shows conus ( a thin hyperreflective arc adjacent to the disc) and pigmentation. subalbinism is common in white and siamese cats with blue irides with obvious choroidal vasculature.

158

What is taurine deficiency retinopathy?

Taurine deficiency causes retinal degeneration and dilated cardiomyopathy in the cat. this condition is now very rare in cats fed proprietory brands of cat food, but may occasionally be recognised in cats fed bizarre diets. Dog food does not contain adequate levels of taurine for cats. the retinal degeneration initially appears as a bilaterally symmetrical hyperreflective band in the area centralis, which extends medially over time until total diffuse retinal degeneration occurs. this esion is ocasionally seen in cats fed a diet containing adequate taurine which may reflect individual absorption problems.

159

What is generalised retinal atrophy in the cat?

A generalised retinal atrophy progressively slowly to complete blindness often recognised in abysinninan and siamese. mixed breed cats are also affected and are often presented very late in the disease as they cope so well with profound visual impairment.

160

What is hypertensive retinopathy

Freq in older cats. sudden onset visual loss. measure BP. retinal and vitreal haemorrhage, retinal detachment and tortuosity of the retinal arterioles, variation in arteriolar calibre. hypaemia may also occur and iOP should be monitor. systemic blood pressure usually very high. handle with care - risk of cerebrovascular haemorrhage Use amlopidine or enalapril maleate - prognosis with retinal detachment and extensie haemorrhage is poor.

161

What is feline panleucopaenia virus?

Antenatal or neonatal infection with the virus can cause retinal dysplasia with/without cerebellar hypoplasia. cerebellar function necessary for the mance response - kittens with cerebellar hypoplasia may lack a menace response despite being visual.

162

What is enrofloxacin toxicity

Baytril - fluoroquinolone - associated with irreversible retinal pathology and blindness when recommended dose exceeded in cats. appears to be narrow margin of safety.

163

What instruments and materials are needed for lid surgery?

Scissors 10-12 cm siize, round points curved and straight. Forceps - fine toothed forceps e.g adsons. Needle holder - around 12cm ize. uture material - 4/0-6/0 polyglactin - vicryl - persists about 4 weeks or vicryl rapide ideal for lid surgery.

164

How should the skin be prepared for eyelid surgery?

Clipping causes many irritating fragments of hair to be released, which end up in the conjunctival sac. in relatively hairless areas it may be better to avoid clipping all together. If clipping is necessary loose hairs can be retrieved by cleansing with a dilution of 1:3 baby shampoo which will not harm the cornea. The area is then prepared aseptically using non lathering aqueous povidine iodine at a dilution of 1:50. Do not allow knots or hairs to touch the eye. aim for good anatomical and anaesthetic reconstrution. ensure that the cornea can be protected adequately by the lids to avoid exposure probems.

165

What should be taken into consideration for post op?

elizabethan collars rarely required as most patients are more comfortable following surgery than they were before hand. foot bandages can be used as a short term measure when patients are inclined to rub the eye. topical antibiotics for -7 days are sufficient following most minor lid surgery.

166

Describe a medial canthoplasty for brachycephalic breeds

One end of a length of nylon suture material can be inserted into the upper punctum, laid around the conjunctival fornix out of the way and the other end inserted into the lower punctual opening. This allows easy identification of the punctae to avoid damaging. An arrowhead piece of tissue encompassing the medial lid margins and any hair bearing caruncular tissue is incised and then removed using scissors. The taut medial canthal ligament should be sectioned. The wound is closed in a simple continuous pattern working towards the nose, with the starting knot and the initial bites taken deep to the conjunctiva. the needle is then directed through the lid margins to ensure accurate closure and the simple continuous pattern through the skin completes closure. This technique deals with trichiasis ad reduces both corneal exposure and the risk of globe prolapse in these breeds.

167

Describe the excision of nasal folds to treat trichiasis?

Readily performed, the nasal folds are simply excised with scissors. The mattress pattern shown helps direct any knots away from the cornea. Howver, the medial canthoplasty is a better alternative.

168

Describe the anchoring technique for chronic or recurrent prolapse of the nictitans gland

The bite through the periosteum should feel very secure, as though you could lift the dogs head from the table with it. a non absorbable suture is used.

169

Describe the excision of ectopic cilium?

The use of a Chalazion clamp will immobilise the lid and reduce haemorrhage. a wedge or block of tissue containing the cilium and its follicle is sharply excised using a no 11 blade.

170

Describe enucleation

Enucleation in dogs and cats indications include: intraocular neoplasia, chronic glaucoma with irreversible loss of vision and evidence of discomfort, panopthalmitis refractory to treatment, a severe ocular trauuma. Do not hesitate to remove an eye that has no prognosis for vision and appears to be causing the animal discomfort. A retrobulbar nerve block prior to enulceation will reduce postoperative pain. Clamp and section at the optic nerve - no need to ligate. Do not apply tension to the optic nerve.

171

How is the eye examined?

Comfort - does it hurt, vision - can the patient see? appearance - does it look normal. Obtain a history, then assess comfort and vision in every patient. Assess the appearance and associated structures under room light and perform a thorough pentorch and Opthalmoscopic examination in a darkened room. the remainder of Occular examination is tailored to the individual patient, not forgetting to complete general examination. Assessment of cranial nerves II - VIII, measurement of tear productio, measurement of intraocular pressure, orbit, globe position, lids and third eyelid, ocular surface conjunctiva, tear film and cornea, anterior chamber, iris, pupil and lens, posterior segment - vitreous and fundus.

172

What does the cornea consist of?

Surface layer of stratified squamous epithelium (8-15 layers thick) which is lipophilic and a barrier to water and bacterial
Stromal layer of collagen (905% of total corneal thickness) which is hydrophilic ad will imbibe water and swell if there is a break in either the epithelial or endothelial barrierrs. exposed stroma stains with fluorescin. Basement membrane - with elastic properties.
Endothelial layer - a monolayer of cells which do not undergomitosis and provide a physical barrier and an active metabolic pump to keep water out the stroma.

173

What is diagnostic mydriasis?

Examination of the structures behind the iris is greatly facilitated by use of a topical mydriatic solution to dilate the pupil. tropicamide used most widely. It is a parasympatholytic agent lasts about 4-6 hours. Do not dilate the pupil if the intra ocular pressure is raised as this will further impede the outflow of aqueous at the iridocorneal drainage angle.

174

What is distant direct opthalmoscopy

Used to assess the clarity of structures within the visual axis and is a simple way to look for opacities. The tapetal reflex is seen when a dog or cat looks nto car headlights at night. the pupil is seen filled with colour as light is reflected by the tapetum back towards the observed. opacities of the lens /cornea will appear black against this background coolour. if the lens is opaque then the tapetal reflection will not be seen at all. nuclear sclerosis is recognised as a ring. It looks as though a contact lens has been placed in the pupil - the older the patient the more obvious the ring appears.

175

What is close direct opthalmoscopy?

Used to provide a magnified view of the ocular structures. the magnification of structures behind the patients lens is more impressive than that of strucutres infront of the lens. good way to view he optic nerve head and the detail f small retinal vessels or small fundic lesions. The field of view is very restricted and peripheral fundic lesions are readily missed. Useful tool for examining lens opacities in general practice.

176

What is the slit beam of the direct opthalmoscope used for?

The slit beam setting of the direct opthalmoscope allows you to localise lesions within the anterior segment of the eye, to detect aqueous flare and to visualise changes in contour of the surface of the cornea or lense capsule. hld the direct opthalmoscope close to the patients eye so that the path of light shining towards eh back of the eye is seen. observe the light beam as it travels through the patients lens at an angle of about 60 degrees. The first reflection closest to the light source is from the tearfilm/cornea. then a black space representing the anterior chamber ca be seen. the light is seen as a smoky beam as it travels through the lens from the anterior lens capsule to the posterior lens capsule.

177

What is indirect opthalmoscopy?

The best way to view the fundus. Indirect opthalmoscope consists of a hand held condensing lens and a focal light source. the examiner should stand at arms length, and direct the light through the dilated pupil until the tapetal reflex is seen. the lens is then positioned a few cm infrot of the eye. allows mots of the fundus to be seen at once. The image is projected upside down with right and left transposed

178

When should bacterial culture and sensitivity be performed?

Most frequently indicated in corneal ulceration when there is a corneal infiltrate in the area of the ulcer. the ulcer is rapidly progressing or deep. the edge of the ulcer should be sampled in this situation, not the conjunctiva. Use a mini tip calcium alginate swab moistened with transport medium prior to sampling, plated out asap.

179

How is tear production assessed?

Normal tears are made up of lipid (from tarsal glands), aqueous (from lacrimal and nictitans gland) and mucus ( from conjunctival goblet cells). Keratoconjunctivitis sicca is a common condition in the dog and represents a deficiency in the production of the aqueous portion of the preocular tear film. this is assessed by the schirmer tear tests strips. Sedation, local anaesthetics and parasympathlytic agents will lower values significantly. normal values: dogs 21.9 +- 4, Cat 20.2 +- 4.5.

180

When should conjunctival /corneal cytology be done?

After the application of topical anaesthesia, scrapings may be obtained using the blunt end of a sterile scalpel blade. cytology may be useful in directing initial bacteriology therapy and in the diagnosis of conditions with cellular infiltrates of the ocular surface such as feline eosinophilic keratoconjunctivitis. One stained with diff quik, another with a gram stain, and third saved for special stains. Crapings may also be smeared onto a sterile culture swab and sent to an outside lab for PCR testing for feline herpes virus.

181

What is fluorescein?

A water soluble dye impregnated onto a paper strip, moistened with sterile saline and applied to the occular surface. Used for the detection of corneal ulcers. Test of nasolacrimal patency, tear film break up time, seidel test - for leaking corneal wounds.

182

What is nasolacrimal cannulation?

Upper punctum is cannulated with a lacrimal cannula and a syringe containing 5ml of saline attached. salne should apppear at the lower punctum when the upper punctum is flushed or at the nares when the lwer punctum is occluded by gentle digital pressure through the lower lid.

183

What is tonometry?

the measurement of intraocular pressure. Normal IOP is maintained by matching aqueous outflow to aquous production. It fills the small space between the lens and the back of the iris flowing through the pupil to fill the anterior chamber between iris and cornea. the majority of aqueous outflow int he dog and cat occurs via th iridocorneal angle to the trabecular meshwork within the ciliary cleft. IOP is measured using an indentation , apllanation or rebound tonometer after topical anaesthesia of the occular surface. Done with schiotz tonometer or tonopen - an applanation tonometer measuring force necessary to flatten a small area of cornea. Dog 16.8+/-4.00mmHg, cat 20.2+-5.5mmhg.

184

What are the signs of acute glaucoma?

Pain, visual loss, episcleral congestion, corneal oedema, dilated pupils, elevated IOP. Specialists use gonioscopy - place tiny scope where the irido-corneal drainage angle is to see if it is still viable or not to determine primary gluacoma. if not - secondary glaucoma due to acute uveitis and synechiae blocking drainage angle If there is iridodensis and an aphakic cresent then it is anterior luxated lens. if there is red eye with miosis, aqueous flare, hypopyin and keratic precipiate then most likely acute uveitis. If it is a primary glaucoma then give a prostaglandin analogue like latanaprost which will open up the less used uveoscleral drainage angle and constrict the pupil. carbonic anhydrase inhibitor is mainstay of glaucoma treatment as it decreases aqueous humor production by 40% and beta blocker timolol also decreased aqueous humour production at a much lesser rate than CAI

185

Describe corneal sequestrum

Most common in cat - persian breeds. a black plaque extrudes through the corneal epithelium that causes pain. these lesions are dealt with by keratectomy and then use a conjunctival pedicle graft.

186

What is meant by the term primary closed angle glaucoma?

Primary angle closed glaucoma is when the irido corneal angle (circular recess between base of iris and peripheral cornea) is obstructed without another disease causing the problem. generally it is due to a developmental abnormality making the angle closed naturally or too narrow. anterior lens luxation may protrude forward towards the iris and lay ontop of the dorsal portion in such a way that it prevents fluid from the poserior uvea reaching he anterior uvea to be drained out.

187

What clinical signs may b e present in a 2 year old dog with a retrobulbar abscess. describe the likely radiographic papperance of retrobulbar cellulitis

Exopthalmos, difficulty in digital retropulsion of the globe, third eyelid protrusion, pain on opening the mouth, strabismus, periorbital swelling, conjunctival hyperaemia, lagopthalmus, increased opacity in the orbit of the eye, slight deviation of the orbit, bone destruction, increased effusion.

188

Describe the nature of the visual impairment likely to be seen with progressive retinal atrophy, describe the fundoscopic appearance at advanced stage of the disease

The owner would most likely say the dog will see fine during the day but will begin to lose confidence by dusk until night falls and the dog cannot see. the rods are lost first then the cones. the Fundoscopic exam will reveal retinal vessel attenuation, hyper reflectivity from tapetum, pavementing, loss of pigmentation from RPE/non tapetal fundus.

189

What tests and procedures would you carry out to diagnose chronic renal failure?

Check serum creatinine levels for function of kidney as creatinine is excreted at a constant ratee and should be filtered out. check for proteinuria to see if proteins are being lost due to excess glomeruli loss. check blood pressure to see if the kidney is becoming hypertensive in order to increase GFR to maintain whatever normal function it can and other oorgans become affected by this as well. some other tests that can be performed are urinarlysis, abdominal radiographs, haematology and biochemistry and ultrasound. renal biopsy should only be used if a mass is encountered. always check weight and body condition score to monitor the progression of the disease as cats lose weight quickly in later stages of CKD.

190

What investigation should be done in kidney disease?

Urinalysis to confirm presence of dilute urine. urine culture also recommended. UPC should be performed to assess for proteinuria. blood pressure measurement should ideally be performed prior to blood sampling, particularly if there is suspicion from the physical examination that the patient may be hypertensive. routine biochemistry will confirm the presence of azotaemia. particular note should also be made of calcium and phosphorus levels and electrolytes. routine haematology useful to assess if anaemia is present as this is associated with a poorer prognosis.

191

What are the potential causes of pituitary and nephrogenic diabetes insipidus in dogs?

Pituitary a non functional tumour on the posterior portion of the gland so no ADH production, congenital, trauma, inflammation. nephrogenic - CKD, liver disease/failure, amphotericin B, vinblastine, hyperhypadrenocorticism, hyperthyroidism, hypercalcaemia, pyometra, pyelonephriitis, glucocorticoids.

192

A dog is presented to you with PUPD. it is hypercalcaemc. what are the DDx for this finding? How would you attempt to diagnose the underlying cause?

Primary hyperparathyroidis, pseudohyperparathyroidism, pancreatitis, addisoons disease, primary hyperparathyroid - urinalysis, take bloods, assess to see if there is high serum PTH with high calcium levels. pseudohyperparathyroid - radiograph to find any evidence of metastasizing neoplasia. bloods to check foor high PTHrp to high calcium. Pancreatitis - radiograph, PLIi, abdominal pain. Addisons - low basal cortisol levels, ACTH stimulation test show sub normal response.

193

Describe the approach to the diagnosis and management of a 4mm diameter desemetocoele iin the central region of the cornea of a middle aged bracycephalic dog.

If an ulcer extends through the full thickness of the stroma to descemets membrane the cornea is in imminent danger of rupture. Suspect a descemetocoele if the centre of the ulcer appears clear (non stroma remaining to be oedematous) . the centre of the ulcer is usually at the base of an obvious depression but in some cases descemets membrane may baloon forwards. Descemets membrane repells the stain. Treatment - left untreated - would heal quickly, but infections are serious so topical broad spec antibiotics (polymixin B) should be applied untill the cornea is fluorescein negative. in under run ulcers - push back edge of ulcer with dry sterile applicators. Midstromal ulcers can be managed with antibiotics and treat reflex uveitis with atropine as needed to dilate the pupil and anti collagenase. Deep ulcer - cytology and culture should be performed, the edge of the ulcer is swabbed then gently scraped back using the blunt end of a scalpel blade. best performed under sedation or GA to reduce the risk of perforation., followed by surgery to support the cornea - conjunctival pedicle graft or corneal conjunctival transposition.Treat empirically with a topical fluoroquinoloone.