opthamology Flashcards
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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
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.
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.
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.
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.
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.
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.
What is a corneal arcus?
Bilateral peripheral lipid deposition, uncommon, invariably associated with plasma hyperlipoproteinaemia and the underlying cause should be determined.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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 .
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What are the guidelines for management of glaucoma depending on underlying cause?
- 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.
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.