Uveal Tract & Glaucoma Flashcards
1
Q
What are the 3 layers of the uveal tract?
A
Iris, Ciliary Body, Choroid
1
Q
Which structures make up the anterior uvea?
A
Iris + Ciliary Body
2
Q
What structure is also known as the posterior uvea?
A
Choroid
3
Q
What are the functions of the 3 structures of the uvea?
A
Iris = regulation of light entering the eye (sphincter and dilator musculature)
Ciliary body = production of aqueous humour to maintain IOP, facilitates lens accommodation and aqueous humour drainage through the iridocorneal angle.
Choroid = thin vascular tunic lining the inner aspect of the globe, rich blood supply - ensures optimal nutrition and oxygenation to the outer retina.
Immunosensitive making it a common site for inflammatory response in the eye.
4
Q
Describe the embryological steps that occur to form the uveal tract.
A
Day 19 post fertilisation
1. Optic cup invaginates creating bilayered medullary epithelium
2. Innermost (vitreal side) differentiates into the inner pigmented epithelium of the iris and non pigmented ciliary body and neurosensory retina
3. Outermost (scleral side) - outer pigment epithelium of iris (dilator and sphincter muscles), pigmented epithelium of ciliary body and the retinal pigment epithelium (RPE)
4. Closure of optic cup occurs via fusion of optic fissure allowing IOP to be established (optic fissure lies in 6 o clock positon - failure of fissure to close = colobomas affecting iris, choroid and optic nerve)
5
Q
What is the difference between a typical coloboma and an atypical coloboma?
A
Typical coloboma = failure of optic fissure to close during development at 6 o clock position
Atypical coloboma = occur away from 6 o clock position and occur through different mechanism.
6
Q
Which uveal structures develop from the neural ectoderm?
A
Posterior iris epithelium
Bilayered ciliary epithelium
7
Q
Which uveal structures develop from the neural crest?
A
Stroma of iris, ciliary body and choroid
Ciliary muscles
8
Q
Which uveal structure develops from the mesoderm?
A
Vascular endothelium
9
Q
How can developmental abnormalities of the uvea be divided?
A
Incomplete development - e.g colobomas
Maldevelopment - e.g anterior segment dysgenesis
Incomplete regression - e.g persistent pupillary membranes
10
Q
What is Collie Eye Anomaly typically associated with? What do the DNA tests for this condition check for and why is litter screening still important for these at risk breeds.
A
Choroidal hypoplasia (always bilateral)
Coloboma of optic nerve (can be unilateral)
DNA test = only detects choroidal hypoplasia - can be negative and still have coloboma of optic nerve
Litter screening 6-7 weeks old
(later than this can appear to ‘go normal’ = choroidal hypoplasia harder to see as tapetal reflection develops at 11-12 weeks.
A lot of dogs do not have both coloboma and choroidal hypoplasia
Mild = no visual deficit
Coloboma = risk of retinal detachment/glaucoma
11
Q
What types of persistent pupillary membranes can be seen and how are they differentiated from anterior synechiae?
A
Iris to Iris
Iris to lens
Iris to cornea
Remnants = speckles
PPM’s always originate from iris collarette
12
Q
How is the iris divided in terms of anatomy?
A
Peripheral ciliary zone
Central pupillary zone
Iris collarette = transition between the two zones and the origin of pupillary membrane remnants.
13
Q
How does the peripheral iris attach to the sclera?
A
Peripheral iris attaches to sclera at region of limbus via pectinate fibres comprising the pectinate ligament.
(Important in glaucoma = pectinate ligament issues = goniodysgenesis)
14
Q
What makes up the majority of the iris and how does this differ between the anterior and posterior iris?
Why is this anatomy clinically important?
A
Majority of iris = stroma, no epithelium to its surface
Modified stromal border forms anterior aspect.
Clinically important - pre-iridial fibrovascular proliferation (PIFM) formation and chronic intraocular disease (described clinically as rubeosis iridis)
New vessels and fibroblasts of fibrovascular membrane do not have to penetrate an epithelium as would be required at other intraocular sites of fibrovascular proliferation.
PIFM’s = major cause of reduced AH drainage and secondary glaucoma in dogs/cats
Posterior aspect lined by pigmented bi-layered epithelium that is continuous with pigmented/non pigmented bi-layered epithelium of ciliary body.
15
Q
Where does the dilator muscle of the iris originate?
A
Dilator = anterior epithelial layer of bilayered posterior epithelium of iris
Is actually a myoepithelium and acts as the dilator.
16
Q
Where does the sphincter muscle of the iris originate? How does the arrangement of this muscle vary between dogs and cats?
A
Stroma close to the pupillary margin - smooth muscle fibres of iris sphincter.
Dogs = circular arrangement
Cats = longitudinal arrangement
17
Q
How is blood supplied to the iris and how is blood drained from iris?
A
Blood supply = long posterior ciliary arteries which lead to major arterial circle (3 and 9 o clock positions)
Drainage = anterior choroidal circulation
18
Q
How are the iris sphincter and dilator muscles innervated?
A
Sympathetic = pupillary dilation via iris dilator muscle (first, second and third order neurons)
Parasympathetic = pupillary constriction via iris sphincter muscle (oculomotor - CN III)
19
Q
Describe the anatomy of the ciliary body.
A
Continuation of posterior aspect of iris
Triangular shape in cross section
Smooth muscle (parasympathetically controlled), connective tissue, blood vessels and nerves
Also makes up uveal part of iridocorneal drainage angle in the form of the uveal trabecular meshwork posterior to the pectinate ligament within the ciliary cleft.
Inner aspect (vitreal side) - lined by inner non pigmented and outer pigmented epithelium
Inner surface divided into pars plicata anteriorally, pars plana posteriorally
20
Q
What is found on the pars plicata of the ciliary body?
A
Heavily folded surface - ciliary proccesses
Flatten out posteriorly at junction with pars plana.
Lens zonular fibres originate from tips and valleys of the ciliary processes and insert adjacent to lens equator therefore suspending the lens caudal to the iris and pupil.
21
Q
Describe the blood supply to the ciliary body.
A
Supply = major arterial circle of the iris
Drainage = anterior choroidal vessels to the vortex veins
22
Q
What are the 3 processes which are required for the production of aqueous humour in the ciliary body? Where do they take place?
A
- Diffusion
- Ultrafiltration
- Active secretion
Take place at the level of the non pigmented epithelium
23
Q
What is the main conventional outflow drainage path for aqueous humour?
A
Conventional outflow = via iridocorneal angle and uveal trabecular meshwork
24
What percentage of aqueous humour outflow is via the non conventional (uveoscleral route) in dogs and cats?
Dogs - 15%
Cats - 3%
25
How may contraction of the smooth musculature of the ciliary body lead to increased AH outflow via the conventional pathway?
Contraction - provides accommodation by moving lens forwards and increasing lens curvature
(This is very limited in dogs and cats however)
26
How is the choroid subdivided into layers? List them in order from outside to inside.
1. Suprachoroideae
2. Large vessel layer
3. Medium vessel layer
4. Choriocapillaris
5. Bruch's membrane
27
Where does the choroid extend to and from and what is it sandwiched between?
From ora ciliaris retinae to optic nerve head
Sandwiched between retinal pigmented epithelium (inner) and sclera (outer)
28
How is blood supplied to and from the choroid?
Short and long posterior ciliary arteries
Venous drainage = via vortex veins
29
What is the aim of the blood-ocular barrier?
Ensure retinal nutrition whilst minimising entry of substances into the eye which may interfere with transparency of the ocular media.
Contributes to ocular immune privilege
30
How is the blood-ocular barrier subdivided?
Blood - aqueous barrier
Blood - retinal barrier
31
What comprises the blood-aqueous barrier?
Tight junctions in non pigmented ciliary body epithelium + pigmented posterior iris epithelium and non fenestrated blood vessels of the iris.
Due to high surface area of ciliary processes the non pigmented epithelium of the ciliary body plays a major role in this barrier.
32
What comprises the blood-retinal barrier? What can be used to test the integrity of this barrier?
Tight junctions in the retinal pigment epithelium
Fluorescein angiography can be used to test integrity.
33
What other elements are there to immune privilege of the eye?
1. Blood-ocular barrier - subdivided into blood-aqueous and blood-retinal barriers
2. Aqueous humour composition - ascorbic acid and other antioxidants
3. Anterior chamber associated immune deviation (ACAID) - spleen associated, antigen detected in eye - activated antigen presenting cells migrate to marginal zone of spleen. Production of antigen specific T regulatory lymphocytes that return to eye and reduce delayed type hypersensitivity.
4. Lack of intrinsic lymphatic system
34
What occurs when ocular immune privilege systems fail or become overwhelmed?
UVEITIS!
Ocular immune privilege systems overwhelmed or fail = breakdown of blood-ocular barrier and clinical signs of uveitis
35
What are the 3 basic events that comprise inflammation of the uvea?
1. Increased blood supply
2. Augmented vascular permeability
3. White blood cell migration
36
What the developmental abnormalities of anterior uveal tissue seen in dogs?
Heterochorma iridis
Subalbinism
Merle ocular dysgenesis
Persistent Pupillary Membranes
Aniridia/iris hypoplasia/coloboma
Anterior segment dysgenesis
37
What acquired conditions can be seen in the anterior uveal tissue of dogs?
Iris atrophy
Iris melanosis
Iridociliary cysts
Uveitis
Intraocular haemorrhage
Ocular melanosis
Neoplasia
38
What is heterochroma iridis?
Normal variation whereby there are different colours within the same iris or two irides.
May occur as manifestation of colour dilution in some breeds e.g Husky or may be associated with colour dilution genes such as Merle and be accompanied by multiple ocular defects (Merle ocular dysgenesis)
Distinguish from acquired colour changes due to uveitis or neoplasia.
39
What is subalbinism?
Another variation of normal - dilution of ocular pigmentation
Blue iris and red fundus reflex
Non pigmented fundus with visualisation of the choroidal vessels
Separate to complete albinism which is not reported in dogs and cats which the eye lacks all pigment.
40
Describe Merle Ocular Dysgenesis. Which breeds are predisposed?
Breeds = Australian Shepherd, Great Dane, Old English Sheepdog, Rough and Smooth Collies
Multiple ocular abnormalities associated with the Merle gene
Individuals carrying two copies of the dominant gene (homozygotes) = most severe ocular abnormalities and an excessively white coat.
Uveal abnormalities - heterochromia iridis, iris hypoplasia, PPM's, corectopia (non central pupil), dyscoria (misshapen pupil), black rimmed pupil (from prominent iridial pigmented epithelium), iris coloboma, choroidal coloboma, choroidal hypoplasia, equatorial staphyloma (protrusion of uvea through scleral defect)
Non uveal abnormalities - microphthalmos, cataract, scleral ectasia (scleral defect), retinal dysplasia and retinal detachment.
Varying degrees of deafness also associated with this condition.
41
What is aniridia/iris hypoplasia/iris coloboma?
Aniridia = born without an iris (very rare)
Hypoplasia - can be partial (focal thinning of iris) or total (full thickness coloboma)
Typical iris coloboma = 6 o clock position
Atypical = positioned elsewhere
42
What does pseudopolycoria describe?
Term used where appears there are additional pupils due to iris coloboma (full thickness)
43
What may occur is cases of iris coloboma where this extends to the ciliary body?
Adjacent lens periphery is abnormally shaped due to lack of zonular fibres - incorrectly referred to as lens coloboma.
44
What is the role of the pupillary membranes during ocular development. How do PPM's occur and present?
Anterior tunica vasculosa lentis and pupillary membrane provide nutrition to the developing lens and anterior chamber in utero.
Should start to regress pre-partum and have fully regressed by 6 weeks post partum.
Incomplete regression = persistent pupillary membrane
Typical PPM's = strands of iris tissue ORIGINATING FROM IRIS COLLARETTE can insert on:
Iris
Lens
Corneal endothelium
(Free floating PPM's can also occur)
Clinically insignificant - remnants, iris to iris and free floating
Iris to cornea - focal corneal oedema (progressive = topical hyperosmotic ointments may be beneficial)
Iris to lens - cataract
45
What is anterior segment dysgenesis?
Malformation of the anterior segment and usually associated with microphthalmos
Faulty separation = corneal, iris, lens and iridocorneal drainage angle abnormalities e.g iris sheet of tissue adherent to cornea, shallow anterior chamber, cornea to lens contact, lens malformations, cataract and glaucoma.
46
What is Peter's Anomaly?
Iris to Cornea PPM is present in combination with defect in posterior corneal stroma, descemet's membrane and endothelium
47
Which main differentials should be considered when you observe iris to cornea PPM's, Peter's Anomaly or anterior segment dysgenesis?
Which differential should you consider for iris to iris PPM?
Which differential should you consider for PPM remnants?
How can you differentiate these conditions?
Iris to cornea PPM ddx =Previous penetrating corneal trauma.
Anterior synchiae associated with prior corneal trauma - span pupil margin towards a full thickness corneal scar (dyscoria)
Iris to lens PPM = ddx posterior synechiae
Posterior synechiae originate on pupillary margin/posterior iris surface only
PPM remnants = ddx iris rest
Iris rest (post inflammation) = peripheral and always black in colour
PPM remnant = light brown and central position
48
What is iris atrophy? How does it appear and which reflex may be affected.
Most commonly result of aging in dogs
Thinning of the iris - often diffuse but can be localised
Any breed can be affected
Pupils may appear dyscoric, dilated and have reduced PLR's.
Photophobia can present in severe cases.
Can occur asymmetrically resulting in anisocoria.
Secondary iris atrophy can occur following trauma, chronic uveitis or glaucoma.
49
What is iris melanosis - what differentials would you consider?
Iris melanosis = focal iridial hyperpigmentation that is of no clinical significance
Flat and not raised lesions
Do not progress or change over time.
Main ddx - anterior uveal melanoma and ocular melanosis
50
What are iridociliary cysts and where do they originate from? What treatment options are there?
Can be congenital or acquired
Arise from posterior pigmented epithelium of iris or from inner non pigmented ciliary body epithelium
Generally benign
Occasionally can interfere with AH outflow or adhere to lens/cornea causing opacification.
If causing obsruction/opacification tx = deflation of cysts via FNA or irrigation/aspiration or laser ablation
(specialist)
51
How can you differentiate an iridociliary cyst from an iridociliary tumour?
Transillumination is required
Bright light source will transilluminate cysts with the aid of the tapetal reflex.
Transparent = cyst
Opaque = mass
52
Define anterior vs posterior uveitis vs panuveitis.
Uveitis = inflammation of the uveal tissue
Anterior uveitis = inflammation of the iris/ciliary body
Posterior uveitis = inflammation of the choroid
Panuveitis = inflammation of all 3 portions of the uvea
53
What are the clinical signs seen with uveitis. Divide them into specific to uveitis and non specific to uveitis.
Specific:
Photophobia
Aqueous flare (pathognomonic for uveitis) 'Tyndall effect'
Anterior chamber cells
Anterior chamber fibrin (often cats)
Keratic precipitates
Hyphaema (other ddx - coagulopathies, systemic hypertension, trauma, A.vasorum)
Hypopyon
Iris swelling
Rubeosis iridis
Iris nodules (other ddx iris neoplasia)
Miosis (other ddx - Horners)
Reduced IOP
Non specific:
Corneal oedema
Blepharospasm
Epiphora
Conjunctival and episceral hyperaemia
Chemosis
Ciliary flush
Pain
Decreased vision
54
List the possible sequelae to uveitis.
Persistent corneal oedema +/- bullous keratopathy
Posterior synechiae (iris to lens)
Dyscoria/restricted pupil movement
Peripheral anterior synechiae
Pigment on anterior lens capsule
Pre-iridial fibrovascular membranes (PIFMS)
Ectropion uveae - PIFM contract and pull pupil outwards
Iris bombe - synechiae all way around, trapped fluid from ciliary body - bulging of iris forwards and secondary glaucoma
Glaucoma
Iris atrophy
Iris cyst formation
Cataracts
Lens luxations - breakdown of zonules
Vitreal degeneration
Retinal detachment
Phthisis bulbi - end stage eye, often glaucoma before, ciliary body stops producing AH and eye shrinks
Blindness
55
List the possible causes of uveitis in dogs.
1. Traumatic - blunt vs penetrating
2. Immune mediated - cataract (phacolytic), lens capsule rupture (phacoclastic), uveodermatological syndrome
3. Metabolic - hyperlipidaemia
4. Infectious
- Viral = Canine adenovirus 'blue eye'
- Rickettsial = Ehrlichia canis, Rickettsia rickettsii
- Bacterial = bacteraemia (pyometra), Borrelia burgdorfei (Lyme's disease), Brucella canis, Leptospira
- Protazoal - Toxoplasma, Neospora, Leishmania
- Fungal - Cryptococcus, Aspergillus, Blastomyces, Coccidiodes, Histoplasma
- Parasitic - ocular larval migrans (toxocara), ocular filariasisis (angiostrongylus vasorum), ophthalmyaiasis interna (Diptera spp), Onchocerca spp
- Algal - Prototheca spp
5. Neoplastic
Primary intraocular - melanoma, iridociliary adenoma/adenocarcinoma
Multicentric - lymphoma, histiocytic neoplasia
Metastatic
Paraneoplastic- hyperviscosity syndrome
6. Miscellaneous
Idiopathic
Breed Related = Golden Retriever Pigmentary uveitis
Ulcerative keratitis (any cause)
Drug induced (Prostaglandin analogues)
56
Describe the typical steps in work up of a canine case of uveitis.
1. Clinical history - known trauma, travel hx, concurrent diseases, neutering status, general health, parasite control.
2. Complete PE to assess patient systemically - e.g evidence of pyrexia, neoplasia (generalised lymphadenopathy), pyometra (discharge) etc
3. Complete ophthalmic examination
4. Initial work up:
Haematology/biochem/urinalysis +/- culture if in house analysis suggestive of UTI
Infectious disease screening - Ehrlichia/Borrelia PCR testing, +- Leishmania PCR if travel hx, serology for Toxoplasma/Neospora)
If history/PE suspicious for concurrent systemic disease may also perform
5. Diagnostic imaging - chest radiography/CT
Abdominal ultrasound
+/- FNA of any abnormal tissues or biopsy
Systemic blood pressure measurement (in cases of intraocular haemorrhage)
Faecal analysis - specifically looking for angiostrongylus vasorum (direct examination)
Aqueocentesis and cytology and not without risk - exception being where strong evidence of lymphoma
Diagnostic enucleation and histopath - reserved for irreversibly blind and painful eyes.
57
When is further more widespread investigation warranted in cases of uveitis?
Bilateral uveitis - especially if presenting with acute, synmmetrical onset of disease
Abnormal PE suggestive of systemic disease
Posterior uveitis
Hyphaema
Severe uveitis - especially before considering immunosuppressives
58
In the UK are dogs or cats more likely to have infectious causes of uveitis?
Cats = mostly infectious
Infectious causes less common in dogs by comparison.
59
What are the two types of trauma? How does their prognosis compare and how can they present?
1. Blunt trauma = poor prognosis generally for both vision and comfortable eye.
Globe rupture possible - usually equator or posterior pole
Signs of rupture = globe collapse, very low IOP, chemosis, hyphaema and subconjunctival haemorrhage. Ocular ultrasound can help confirm and may also reveal retinal detachment, cyclodialysis (separation of iris and ciliary body from sclera), lens luxation, hyperechoic opacities in posterior segment and ill defined scleral borders.
Absence of dazzle = poor prognostic indicator
Enucleation often tx of choice in severely traumatised, blind eyes.
2. Penetrating trauma
All should be treated with topical and systemic AB's - endophthalmitis = possible sequelae
Uncomplicated punctures - small punctures will self seal and require symptomatic medical therapy in form of topical antibiotics, mydriatics and anti-inflammatories + systemic antibiotics and anti-inflammatories.
Careful assessment of lens capsule integrity important following mydriasis.
Penetrating trauma with lens injury - phacoclastic uveitis complicatiom. >2mm injuries = early lens removal via phacoemulsification
Small capsular tears <2mm may self seal and can oftne resolve following prompt medical tx.
Lens involved = risk of septic implantation syndrome - impregnation of bacteria into lens which then acts as growth medium - endophthalmitis
Can have delayed onset for septic implantation syndrome = 10 days to 1 year reported.
Cats = also risk of post traumatic sarcoma development following lens injury and ocular trauma.
Penetrating wounds with iris prolapse
Larger perforations iris may be pushed forwards into defect and may temporarily seal
Acute cases <24hrs - reposition iris and globe repair should be performed
Chronic wounds = increased risk of infection and suppurative endophthalmitis
Ocular foreign bodies
DO not grasp with forceps - can push further into cornea/anterior chamber
Perpendicular removal with foreign body spuds/needles
Iatrogenic globe perforation - maxillary tooth removal, often associated with retinal detachment and endophthalmitis. Poor prognosis.
60
What is septic implantation syndrome?
Bacteria implanted directly into lens during full thickness corneal perforation (often cat claw injuries)
May initially respond well to medical therapy however following period of latency (often months) a severe secondary endophthalmitis develops and the globe then requires enucleation.
61
What are the 2 main types of lens induced uveitis? Why do they occur?
Likely that in the normal lens small amounts of lens protein (which is weakly antigenic) escape and induce T cell tolerance. This tolerance is overwhelmed when the immune system exposure to crystallins is increased by cataract formation, lens trauma or lens capsular rupture leading to uveitis.
1. Phacolytic uveitis = lens capsule intact
All stages of canine cataract = some form of subclinical uveitis
Rapidly progressive cataracts e.g diabetic cataracts often display severe secondary uveitis and prompt medical tx (topical and systemic anti-inflammatories) + phacoemulsification is vital
Failure to do so = lens capsular rupture, retinal detachment and secondary glaucoma preventing from being candidate for cataract surgery.
2. Phacoclastic uvieits = ruptured lens capsule
Either due to trauma or spontaneous rupture (rapidly progressive cataract)
Large amounts of lens capsule material overwhelms T cell tolerance leading to severe uveitis.
Early referral for phacoemulsification is essential in cases of lens capsule rupture.
62
Describe uveodermatological syndrome - how is it treated and which breeds are predisposed?
Immune mediated condition - destruction of melanocytes in eyes and skin
Vision and globe threatening
Akitas, Huskies and other larger breeds predisposed
Ocular signs = severe panuveitis, retinal detachment, glaucoma
Skin and hair depigmentation around face and genitals but can be more diffuse.
Crusting around mucocutaneous junctions
Diagnosis - signalment, clinical signs, skin biopsy (histopath = granulomatous inflammation around pigmented cells)
Tx = aggressive immunosuppressives
Oral prednisolone + azathioprine or ciclosporin
Topical tx - frequent corticosteroids +/- anti glaucoma treatment
Prognosis for vision/globe = poor
Often develop secondary refractory glaucoma
Lifelong treatment always required.
63
How may hyperlipidaemia lead to uveitis in dogs? Which breed is predisposed? What can be seen as a rare complication?
Lipid influx into anterior chamber - lipid-laden AH when there is a breakdown of the blood-aqueous barrier (anterior uveitis) and concurrent hyperlipidemia.
Systemic work up required to identify and treat cause of hyperlipidaemia.
Minature Schnauzers = occurs more commonly alongside idiopathic uveitis
Rare complication of hyperlipidaemia = intraocular tumour - Xanthogranulomas (Miniature Schnauzers that suffered from diabetes and hyperlipidemia)
64
How does infectious canine hepatitis (adenovirus) cause uveitis?
Uncommon now due to routine vaccination
Uveitis induced by type III hypersensitivity involving immune complexes.
Unvaccinated/younger animals predisposed
Classical signs of uveitis + often severe corneal oedema and thickening relating to corneal endothelial dysfunction.
Tx = symptomatic medical therapy (topical and systemic)
65
What are the 2 Rickettsial causes of uveitis in dogs? How are they spread?
How are they diagnosed and treated?
1. Ehrlichia canis - tick borne disease, obligate intracellular microrganism. Preferentially infects thrombocytes so ocular signs usually associated with intraocular haemorrhage. Other signs = retinal detachment, optic neuritis and panuveitis.
Diagnosed via PCR of whole blood
Tx = oral doxycycline 5mg/kg for 3 weeks + oral prednisolone 0.5mg/kg/BID
Anterior uveitis only = better prognosis
2. Rickettsia rickettsii - Rocky Mountain Spotted Fever
Tick borne disease prevalent in USA. More mild ocular signs
Diagnosis = paired serology
Tx= doxycycline for 3 weeks as above
66
How can bacteraemia cause uveitis?
Any bacteraemia e.g due to pyometra/periodontal disease can cause uveitis if there is dissemination of bacteria into the uveal tissues and production of circulating endotoxins.
67
How does Lyme's disease (Borrelia burgdorfei) present and what is the treatment?
Endemic to UK but rare cause of uveitis in dogs
Uveitis + signs of systemic illness = should be PCR tested
Other clinical signs = lymphadenopathy and lameness
Tx = oral doxycycline
68
How does brucellosis present as a cause of uveitis in dogs, how is it diagnosed?
Imported animals
Ocular signs = anterior uveitis, endophthalmitis, chorioretinitis, keratoconjunctivitis, hyphaema
PCR = definitive diagnosis
Notifiable disease
69
How does leptospirosis present as a cause of uveitis in dogs. How is it treated?
Not very common due to vaccination
Vasculitis = kidney and liver failure
Anterior uveitis, hyphaema and retinal detachments have all been reported but ocular signs less common manifestation of this type of disease.
70
How does Toxoplasma gondii present as uveitis in dogs? How is it diagnosed and treated?
Often subclinical uveitis - less common cause than in cats
Routes on infection = ingestion of cat faeces (sporulated oocytes), ingesting tissue cysts in intermediate hosts, infected meat and transplacentally.
Ocular signs = keratoconjunctivitis sicca, episcleritis, anterior uveitis, chorioretinitis, optic neuritis and polymyositis.
Diagnosis = Paired serological samples (IgM and IgG)
Tx = Clindamycin for 4 weeks
71
How does Neospora caninum present as uveitis in the dog?
Ocular signs - retinitis, choroiditis, iridocyclitis and extraocular myositis
Often most common clinical sign = hindlimb paralysis
72
How does Leishmania infantum present as uveitis in the dog? How is it diagnosed and managed?
Often dogs with travel/import hx.
Endemic areas - Mediterranean, Africa, India, Americas) - transmitted by sandflies
Long incubation 3-4 years
Ocular signs - blepharitis, KCS, uveitis, retinitis, endophthalmitis
Usually also systemic signs = lymphadenopathy, splenomegaly, hepatomegaly, renal failure, anaemia, thrombocytopaenia and dermatological conditions.
Diagnosis = serology, PCR (blood, aspirates, biopsy) or histological identification of the organism.
Management = systemic antiprotazoal and topical anti-inflammatories +/- systemic corticosteroids
Relapses common occurring years after the discontinuation of treatment.
73
How do fungal diseases in dogs present with uveitis?
Rare in UK - often imported dogs
Inhalation = primary route of infection with haematogenous spread to the eye
Typically pyogranulomatous uveitis with posterior segment disease
Cryptococcus - CNS, ocular, respiratory and cutaneous signs, diagnosis = antigen serology, tx = systemic antifungals, prognosis = poor due top severity of meningoencephalitis
Aspergillus - GSD predisposed, ocular signs accompany severe systemic illness
74
What are the parasitic causes of uveitis in dogs and how do they present?
Ocular nematodes = Toxocara Canis L2, focal granulomatous fundic lesions and may be associated with more extensive retinal degeneration
A.vasorum = subconjunctival haemorrhage to severe granulomatous uveitis
L3 sometimes visualised in vitreous
Systemic signs associated with coagulopathies/coughing
Killing the parasites can make the uveitis worse and if the larvae are accessible surgical removal should be considered.
Dirofilaria immitis - not in UK but consider in imported dogs
Dipteran larvae migration - not reported in UK
Onchocerca - granulomatous episcleral lesions, associated anterior and posterior uveitis. Confined to Meditteranean and not reported in UK.
75
How does algal uveitis in dogs present?
Prototheca - algae that lack chlorophyll - haemorrhagic diarrhoea in dogs
Ocular signs = anterior uveitis, secondary glaucoma, chorioretinitis and retinal detachment.
Prognosis = poor prognosis for survival
Tx with itraconazole can be attempted.
76
In which cases should uveal neoplasia in dogs be considered?
Consider in cases with intraocular masses, haemorrhage, glaucoma and retinal detachment - particularly older patients.
77
Which primary intraocular tumours in dogs can lead to uveitis and how do they present?
How are they treated?
1. Melanocytic tumours - most common intraocular tumour in the dog, majority are benign and originate from anterior uvea. Even of malignant forms histologically very few metastasise. Can be locally destructive leading to uveitis and then glaucoma.
2. Iridociliary epithelial tumours - second most common
Adenomas and adenocarcinomas (based off whether scleral invasion occurs) - pigmented or non pigmented masses within pupil. Can lead to secondary glaucoma but rarely metastasise.
Other less common intraocular tumours = medulloepithelioma, spindle cell tumours of iris in blue eyed dogs, haemangioma/sarcoma, leiomyosarcoma.
If not causing uveitis/glaucoma - often benign neglect due to low rate of malignancy/metastasis in dogs.
Tx - smaller well defined tumours - laser diode ablation or surgical excision - (referral to specialist)
Large tumours and/or those with secondary complications - enucleation + histopath (pre-surgical survey diagnostic imaging should be performed if suspect metastatic disease or systemic neoplasia.
78
What types of multicentric/systemic neoplasia may cause uveitis - how are they treated?
1. Lymphoma - 3rd most common intraocular neoplasia in dogs
1/3rd of dogs with lymphoma show ocular signs - anterior uvea including iris infiltration by neoplastic cells.
Clinical signs = hyphaema, accumulation of neoplastic cells in anterior chamber (mimicking hypopyon), iris infiltration. Can also recognise in the retina, optic nerve, peripheral nerve tissue and orbit.
Diagnosis - cytological or histopath identification of neoplastic cells (blood sample, lymph node, organ FNA, aqueocentesis, tissue biopsy)
Tx = treatment of ocular signs is symptomatic as widespread neoplasia so needs to be combined with chemotherapy protocol.
2. Histiocytic neoplasia
Histiocytic sarcoma - unilateral ocular signs = uveitis, secondary glaucoma and intraocular mass.
Breed predisposition = Rottweiler, Labrador, Golden Retrievers.
Detailed work up will often reveal other masses
Prognosis = poor and tx options limited.
79
What intraocular tumours are metastatic in dogs?
Haemangioma/haemangiosarcoma, adenocarcinoma. fibrosarcoma, rhabdomyosarcoma, osteosarcoma, chondrosarcoma, phaeochromocytoma, TVT, cutaneous melanoma, malignant histiocytosis
80
What is hyperviscosity syndrome and how may it lead to uveitis in dogs?
Monoclonal gammopathy associated with lymphoproliferative disorders (e.g multiple myeloma)
Ocular signs generally in posterior segment - retinal vasculature dilation and tortuosity, retinal haemorrhages, retinal detachment, choroiditis and papilloedema.
81
When can you call uveitis 'idiopathic'?
Diagnosis of exclusion - when after extensive work up a cause has failed to be identified
(Idiopathic itself not a true diagnosis and may represent a false negative result, failing to test for causative agent or because uveitis is caused by something not previously reported).
If uveitis is severe then immunosuppression is often required which implies possible immune mediated aetiology.
82
What are the goals of uveitis treatment?
Reduce inflammation, control pain and reduce the risk of sequelae development.
83
How is uveitis generally treated in dogs?
Try to identify underlying cause and target therapy if possible.
Anterior segment structures - reached by topical medications
Posterior segment structures - need systemic
General uveitis treatment:
1. Topical corticosteroids - ok as long as fluorescein -ve, 1% Prednisolone acetate good choice as good corneal penetration achieved
2. Topical NSAID - can be used alongside topical corticosteroids and may have synergistic effect. Ketorolac maleate 0.5% - can also be used alone if ulcerative keratitis present.
3. Systemic NSAIDs - can be used initially until infectious agents ruled out but as can alter platelet function care should be taken if there is systemic coagulopathy present.
4. Systemic corticosteroids - should only be used once infectious disease ruled out (however in some cases immediate treatment required to prevent loss of vision)
Blood samples should be obtained prior to tx and close monitoring of patient recommended.
Client should be warned these are not without risk if there is underlying infectious disease.
Severe and/or immune mediated uveitis - immunosuppressive doses of prednisolone systemically (2-4mg/kg daily divided into doses) - gradually tapered depending on response.
+/- azathioprine (1mg/kg) or ciclosporin (5mg/kg) - helps reduce prednisolone dose and eventual discontinuation of steroids.
Lifelong tx required in some cases
Regular haematology/biochem monitoring important for dogs on immunosuppressive medications.
5. Topical mydriatics/cycloplegics - acute stages of uveitis to reduce posterior synechiae, reduce discomfort from ciliary muscle spasm and help stabilise blood aqueous barrier.
1% atropine - parasympatholytic drug - mydriatic and cycloplegic effects - applied 2-3x daily until maximal dilation then reduce to EOD or every third day
0.5% tropicamide mydriatic only and no cycloplegic effect - 2-3x daily application keeps pupil moving due to relatively short duration of action so can help prevent posterior synechiae formation.
CAUTION - DO NOT USE ATROPINE IN CASES OF UVEITIS WITH SECONDARY GLAUCOMA - MYDRIASIS INCREASES IOP
84
Which breed can get Pigmentary Uveitis and how does it present? What is the prognosis?
Golden Retrievers (occasionally Great Danes)
Pigment dispersion on anterior lens capsules in both eyes
Uveal cysts, fibrinous debris on anterior lens capsule, cataracts and posterior synechiae can all also develop.
Most dogs - aqueous flare but histopathologically degree of uveitis is minimal.
Long term prognosis = poor as often develop refractory secondary glaucoma
Mechanism for glaucoma multifactorial - multiple cysts push iris forwards narrowing ciliary cleft, posterior synechiae formation - iris bombe, PIFM formation, intraocular haemorrhage.
Typically managed = topical NSAID and IOP monitoring
85
How does ulcerative keratitis lead to uveitis?
Axonal reflex which effects blood vessel dilation, permeability and leucocyte chemotaxis.
Secondary uveitis to corneal ulceration often more pronounced in brachycephalics and often may result in associated hypopyon.
86
Which drugs use in canine glaucoma management may cause uveitis? Which other drugs can cause transient breakdown in blood-aqueous barrier?
Topical prostaglandin analogues - latanoprost/travoprost - mild anterior uveitis, strict miosis and iris hyperpigmentation.
Parasympathomimetics (pilocarpine and demecarium bromide) - can cause transient breakdown of blood-aqueous barrier
87
How do iris and cilliary body cysts differ in cats compared to dogs?
Cats - very darkly pigmented so can be difficult to transilluminate, less common, tend to stay adhered to the iris/ciliary body and more obvious following pupil dilation.
Unlikely to progress and cause associated issues with vision/aqueous humour flow.
88
What may be seen in cats with white coats and blue eyes?
May be congenitally deaf - mode of inheritance dominant but split between the coat colour (complete penetrance) and eye colour/deafness (incomplete penetrance) - therefore not all white cars are deaf.
89
What is feline colobomatous syndrome?
Uncommon congenital condition
Upper lateral eyelid agenesis with other intraocular abnormalities including PPM's, uveal/optic nerve colobomas and retinal dysplasia.
(Mustarde technique often used to repair upper eyelid)
90
What is Chediak-Higashi syndrome in cats? Which breed does it affect?
Persian cats - rare syndrome
Light coloured irises, hypopigmentation of non tapetal fundus and tapetal degeneration
Increased susceptibility to infection and bleeding tendency
Diagnosis based on clinical signs, signalment and identification of enlarged melanin granules in the hair shaft.
91
Describe iris melanosis in the cat. What other differentials are there for this pigmentation. How would you approach?
Iris melanosis = spontaneous benign focal areas of iridial hyperpigmentation
Middle aged to older cats generally
Key features:
No effect on pupil motility or shape
Flat and regular appearance
Slow progression
Other ddx - pigmentation secondary to uveitis vs early diffuse iris melanoma
Very difficult to distinguish iris melaonsis from diffuse iris melanoma on examination alone
Recommendation - close continuous monitoring including photo documentation for comparison
92
How do cats and dogs differ in terms of the presentation of uveitis.
Cats = often present later in disease process as clinical signs are more insidious and subtle. Usually present more comfortably with uveitis compared to dogs.
Dogs often very obvious uveitis in acute stages - blepharospasm, pain, photophobia noticed etc.
93
What are the most typical signs of uveitis in cats.
Keratic precipitates (often ventral and may be missed due to position of TEL)
No pain or only mild level of ocular discomfort
Iris hyperpigmentation
Iris neovascularisation (rubeosis iridis)
Aqueous flare
Cataracts
Iridial nodules
Inflammation of the anterior vitreous (pars planitiis and described as 'snow banking')
94
Describe the typical sequelae to uveitis in cats.
Anterior lens luxation
Secondary glaucoma and hydrophthalmos (these globes often still have some vision)
Lagophthalmos and axial ulcerative keratitis
95
List the possible causes of uveitis in the cat.
1. Trauma - blunt or penetrating
2. Immune mediated
Lens related (phacolytic, phacoclastic)
3. Metabolic
Hyperlipidaemia
4. Infectious
Viral - FIV, FeLV, FIP
Bacterial - Bartonella
Protozoal - Toxoplasma gondii, Leishmania infantum
Fungal - Cryptococcus
Lens induced - E.canaliculi
5. Neoplastic
Primary ocular - melanoma, iridociliary adenoma/adenocarcinoma, post traumatic sarcoma
Multicentric - lymphoma
Metastatic- (pulmonary, ulcerative lesions on digit, x-ray chest)
6. Miscellaneous
Lymphoplasmacytic uveitis
Systemic hypertension
96
How would you investigate a case of feline uveitis?
1. Hx - likelihood of prior trauma, concurrent illness, travel history, vaccination status, hunting status, cat fights etc.
2. Full PE - evidence of infection (pyrexia), generalised lymphadenopathy etc
3. Complete ophthalmic examination
4. Initial work up:
Haematology/biochemistry/urinalysis - ensuring measures serum albumin/globulin
Infectious disease screening - FeLV antigen and FIV antibody testing, serology for toxoplasma IgG and IgM, coronavirus antibody titre
5. If history, PE, opthalmic exam or initial bloods suggestive of systemic disease then in addition to above Diagnostic imaging should be performed.
Chest x-rays or CT
Abdominal ultrasound or CT
+/- FNA any abnormal tissues or biopsy
6. Systemic blood pressure (especially in cases of intraocular haemorrhage)
7. Aqueocentesis and cytology - if suspect lymphoma, otherwise little benefit.
8. Diagnostic enucleation and histopathology for irreversibly blind and painful eyes.
97
How does trauma as a cause of uveitis differ in cats compared to dogs?
1. Penetrating traumas less severe ocular signs compared to dogs
2. Cat claw injuries = most common form of trauma - septic implantation syndrome not uncommon with these types of injury if lens damaged.
3. Gunshot injuries - airgun pellets more common than in dogs
4. Feline post traumatic sarcomas can occur years later after a traumatic event and are highly aggressive malignant intraocular neoplasms - consider this fact when deciding whether or not to enucleate a severely damaged globe.
98
What can E.cuniculi cause in cats?
Can lead to cataract formation in cats as well as a secondary uveitis.
Case series - all cats had elevated serum antibody titre levels and positive PCR testing of AH and lens capsule.
Cats respond well to early lens removal in conjunction with oral fenbendazole, NSAIDs and topical corticosteroids.
99
What is the most common category to cause uveitis in cats?
Infectious causes (whereas in dogs often idiopathic uveitis in the UK)
100
How does FIV present in cats with uveitis? How is it diagnosed and what is the prognosis.
Feline Immunodeficiency Virus
Chronic immunosuppression - chronic uveitis
Transmission through bite wounds and saliva
Ocular inflammation either by direct viral damage or by allowing opportunistic infection of the eye (e.g co infection with Toxoplasma)
Ocular signs = anterior uveitis, pars planitis, intraocular lymphoma, CNS related neuro-ophthalmological signs.
Diagnosis = postiive ELISA for antibody (Snap test), can be confirmed with Western blot.
Treatment = palliative and prognosis poor.
101
How does FeLV present in cats with uveitis? How is it diagnosed and what is the prognosis?
Feline Leukaemia Virus
Retrovirus - transmitted vertically and horizontally via body fluids and faeces.
Young cats in multi cat households with poor environmental hygiene at most risk
Clinical signs due to immunosuppression, oncogenesis (lymphoma related) and anaemias.
Ocular signs = uveal, orbital or adnexal lymphoma, anterior uveitis with KP's, chorioretinitis, chorioretinal masses, retinal detachment, optic neuritis, spastic pupil syndrome and CNS related neuro-ophthalmological signs.
Diagnosis = ELISA for FeLV antigen (snap test), which can be confirmed with PCR
N.B positive test does not confirm that ocular disease is as a direct result of the virus
Palliative tx.
Long term prognosis = poor.
102
How does FIP present in cats with uveitis? How is it diagnosed and treated? What is the prognosis?
Feline Infectious Peritonitis
FIP = mutation of very common feline coronavirus (FCoV)
FCoV common in multi-cat households
Majority affected <1 year (up to 12% of FCoV infected cats may go on to develop FIP)
Clinical signs of FIP caused by immune complex disease and pyogranulomatous vasculitis.
Ocular signs bilateral - anterior fibrinous uveitis, prominent KPs, iris swelling, chorioretinitis with perivascular cuffing, exudative retinal detachment, optic neuritis and CNS related signs
Ocular signs in about 9% of wet FIP cases, 70% dry FIP cases
Systemic signs = weight loss, anorexia, lethargy, pyrexia, anaemias, granulomatous lesions affecting multiple organs (dry form) and peritoneal or thoracic effusions (wet form)
Ante mortem diagnosis difficult without biopsy of affected organs but diagnosis often reached based on:
Patient hx and signalment
Clinical signs
Lymphopenia, hyperglobulinaemia, low albumin:globulin ratio, elevated FCoV titre and elevated acute phase proteins.
Treatment can be aimed at controlling the immune mediated disease + antiviral medications - Remdesivir and GS-441524 + supportive care.
Preognosis = guarded to poor
103
How does Bartonella present in cats with uveitis? How is it diagnosed and treated?
Bacterial disease - cat scratch disease in humans
B.henselae common in warmer climates where flea populations are high (mode of transmission)
High prevalence within cat populations so correlating to clinical disease can be challenging
Diagnosis - serum antibody titre + PCR testing on whole blood
AH can also be submitted for PCR testing/antibody detection
C value >3 = local antibody production
Tx for all ill cats with suspected bartonellosis = oral doxycycline 10mg/kg BID for 2-6 weeks
104
How does Toxoplasma gondii present in cats with uveitis? How is it diagnosed and treated?
T.gondii - cat is definitive host
Protazoal
Most common route of infection = ingestion of intermediate hosts infected with bradyzoites in tissue cysts.
Other routes = ingestion of faecal material containing oocysts or transplacentally (tachyzoites)
Cats infected with T gondii may develop ocular signs of anterior uveitis, chorioretinitis, retinal detachment, optic neuritis and extraocular myositis.
Diagnosis can be challenging given high presence of serum antibodies in the general cat population.
Paired serology testing for IgM and IgG recommended
IgG levels may be elevated for years following infection so not an indicator of active infection alone.
Tentative diagnosis made based on:
High IgM titre >1:256
Rising IgG titre
Favourable response to antiprotazoal treatment
AH can be submitted for antibody titres and the Goldmann-Witmer coefficient (C value) can be calculated. >3 = local antibody production
Treatment = clindamycin 12.5mg/kg BID for 4 weeks minimum
Total clearance of infection unlikely
?concurrent use of systemic corticosteroids - risk of reactivation with steroids = unknown
ZOONOTIC DISEASE - pregnant and immunocompromised individuals should be warned.
105
How does cryptococcus present as a cause for uveitis in cats?
Fungal
Most common systemic mycosis in cats worldwide but not very common in UK
Infection usually inhalation through nasal cavity and then dissemination to skin, lungs and lymph nodes, CNS and eyes.
Ocular signs = granulomatous chorioretinitis and optic neuritis as well as uveitis.
Antigen detection in body fluids = diagnosis
106
How does diffuse iris melanoma present in cats? How is it diagnosed and treated? What is the prognosis?
Most common intraocular tumour in cats
Very variable presentation/progression making giving advice on the management of these cases problematic.
Some tumours = enlarge slowly over time and never metastasise whereas others progress rapidly and lead to uveitis, secondary glaucoma and metastatic disease.
Metastasis = most likely to abdominal organs rather than lungs
Ocular signs more consistent with DIM:
Pigmented spots with altered surface texture (velveting) or raised surface
Pupil abnormalities - dyscoria, anisocoria, reduced PLR
Pigmented cellular flare
Progression of the hyperpigmented areas
Associated anterior uveitis and glaucoma
Management options:
1. Close monitoring with photo documentation (if none of the obvious criteria above)
2. Incisional biopsy (but not without risks - specialist only procedure)
3. Enucleation (accepting the risk that lesion could turn out to be benign melanosis)
(Laser ablation not generally recommended in cats with iridial hyperpigmentation)
Iris melanosis can progress to melanoma so always recommended to carefully monitor any cat with pigment change in the iris.
If performing enucleation - thoracic and abdominal imaging also recommended to assess for metastatic spread prior to removing globe.
107
How do post-traumatic sarcomas present in cats. What is the prognosis with these types of intraocular tumours?
3rd most common intraocular tumour in cats
Variants - spindle cell (most common), round cell and osteo/chondrosarcoma variant.
Feline eyes that have sustained prior trauma = at risk, especially if lens capsule was ruptured
Develops months-years after event.
Highly locally aggressive and metastatic risk high - often spread to CNS by time detected.
For this reason prophylactic enucleation of traumatised blind globes is recommended in cats.
108
How do iridociliary adenoma/adenocarcinomas present in cats with uveitis?
4th most common intraocular tumour
Always non pigmented in cats and often cystic
Originate from ciliary body and infiltrate the iris.
109
How does intraocular lymphoma present in cats with uveitis?
2nd most common intraocular neoplasm in cats
Ocular disease may precede systemic signs but is a systemic disease rather than a localised disease process.
Always assume have disseminated disease and stage/treat accordingly (chemotherapy)
Approx 50% of cases occur in conjunction with lymphoplasmacytic uveitis.
Non pigmented appearance with irregular surface.
110
What types of neoplasms may metastasise to the eye and cause uveitis in cats?
Pulmonary carcinomas
Squamous cell carcinoma
Fibrosarcomas
Tendency to affect the choroid rather than anterior uvea
111
What is lymphoplasmacytic uveitis in cats? How does it present and what is the prognosis?
Non specific ocular immune response with unclear aetiology
Often diagnosis of exclusion
Can be unilateral or bilateral
Often relatively resistant to symptomatic anti-inflammatory therapy
Ocular signs - inflammatory iris nodules, KPs, rubeosis iridis, PIFMS, inflammatory debris on lens capsule
Symptomatic anti-inflammatories recommended for these patients (lecturer recommended topical NSAID + systemic NSAID then switch to ciclosporin once all infectious causes ruled out, systemic preds wouldn't be wrong, topical steroids in cats best avoided as high prevalence of herpes virus concurrently)
Long term prognosis = poor due to development of secondary glaucoma due to obstruction of the drainage angle by inflammatory infiltrates or PIFMS + lens luxations
112
What is a major cause of intraocular haemorrhage in cats?
Systemic hypertension
BP measurement should always be included in the work up of any older cat with intraocular haemorrhage.
113
What indications are there for surgery of the iris and who should perform these?
Requires advanced ophthalmic microsurgical skills and operating microscope - referral to specialist.
In reality surgery on iris is rarely performed but possible indications would be:
Iridial mass removal
Posterior synechiae removal
Iridial biopsy
114
What is the major complication that can be anticipated with iridial surgery?
Intraocular haemorrhage (3 and 9 o clock positions in particular should be avoided as where long ciliary arteries enter globe)
115
What possible techniques are there for iris mass removal surgically?
1. Sector iridectomy - focal iris masses (rarely performed as superseded by laser photocoagulation). Initiated by perilimbal corneal incision.
Complications - haemorrhage/incomplete excision of the masss
2. Sector iridocyclectomy - rarely performed, may be used where ciliary body affected also in case of a uveal tumour
3. Laser photocoagulation (used for iris melanoma in dogs) - diode laser photocoagulation is efficient non invasive option for treatment of presumed iris melanoma in dogs.
Some cases require more than 1 treatment but risk of post op complications is low.
116
What possible techniques are there to address posterior synechiae formation and/or improve AH drainage?
Sphincterotomy - during cataract surgery incomplete mydriasis may make delivery of artificial intraocular lens difficult. In these cases iridotomy of the pupillary sphincter may be perfomed by 2x 1-3mm incisions at pupillary margin at 2 and 4 o clock positions.
Synechieotomy/pupil iridotomy - extensive posterior synechiae can occur following cataract surgery and surgery can be performed to disrupt these adhesions.
Direct iridial incisions or Nd:YAG laser in non invasive alternative.
Risk of synechiae re-formation = remains high
Iridotomy - used to make an alternative pathway for AH to flow when flow through the pupil is compromised due to extensive posterior synechiae formation.
Unfortunately holes created by iridotomy are often temporary and close within a few weeks.
117
What indication may there be for iridal biopsy?
Incisional biopsy in cats to determine diffuse iris melanoma from iris melanosis.
Should be performed by specialist if going to attempt
Risk - intraocular haemorrhage/uveitis
Feline iris melanosis can go on to progress and become iris melanoma!
118
What is the normal intraocular pressure range for dogs and cats?
10-25mmHG = normal
Compare both eyes!
119
Define glaucoma.
Glaucoma = complex neurodegenerative disease
High intraocular pressure combined with retinal ganglion cell loss.
120
What pathophysiological changes occur to the eye with glaucoma?
Increased intraocular pressure - due to decreased AH drainage
Outward bowing of the lamina cribosa - leads to compression of retinal ganglion cell axons
Blockage of axonal transport
Eventual death of retinal ganglion cells - blindness
Also decreased perfusion of tissues with increased IOP - further death of cells.
Bystander chain reaction - dying retinal ganglion cells release glutamate, overstimulates the surrounding retinal ganglion cells leading to apoptosis and further cell death.
121
How is a normal physiological IOP maintained in steady state?
Balance between production of aqueous humour (by the ciliary body epithelium) and drainage (via iridocorneal angle)
122
How does aqueous humour usually circulate?
1. AH produced from ciliary body epithelium
2. Circulates along convention currents from the posterior chamber via the pupil into anterior chamber
3. Drained via iridocorneal angle (360 degrees)
4. Passes through trabecular meshwork of iridocorneal angle and is removed via ciliary vein network (conventional pathway - 97% cats, 85% in dogs)
123
Describe the structure of the iridocorneal angle.
Entrance to iridocorneal angle marked by the pectinate ligament - structure of fine fibrils spanning the iridocorneal angle from iris root to endothelial aspect of corneo-limbal junction.
Contains fine network of trabeculae (trabecular meshwork) - through with aqueous humour percolates prior to removal via scleral plexus into ciliary vein network.
124
What is an increase in IOP always representative of physiologically?
Increased IOP = failure of drainage system
(Overproduction of AH has never been documented in canine or feline patients)
125
Why can we visualise the iridocorneal angle in the cat without gonioscopy vs dogs where gonioscopy is required to visualise?
Due to total internal refraction
Cats curvature of the cornea is different to dogs affecting the level of refraction and allow the iridocorneal angle to be viewed with a slit lamp alone.
126
How is glaucoma diagnosed?
Combination of clinical signs/presentation + high IOP on tonometry +/- gonioscopy assessment
127
Describe the different types of tonometers. What are their advantages/disadvantages?
Schiotz tonometer - cheap but more challenging to use
Works by indenting corneal surface with small plunger from footplate which is rested on corneal surface.
Can be performed under topical anaesthesia but patients cornea must be horizontal to obtain readings
Plunger indents cornea is connected to pointer on a scale - these readings are then converted via chart to IOP. Lower readings on scale = higher pressure
Limited use for ulcerated corneas or corneas with extensive surface pathology (e.g very oedematous or with granulation tissue formation)
Tonopen - applanation digital tonometer, converts force required to applanate a small area of the cornea into a digital IOP value.
Measurements taken with topical anaesthesia
Tonovet = rebound tonometer, measures force with which small magnetised probe shot at corneal surface (without need for local anaesthesia) is rebounded.
Converted to mmHg, easy to use but costly.
128
What is gonioscopy? How is it performed.
Procedure to assess the iridocorneal angle
Used to overcome total internal refraction in dogs
Gonioscopy lens applied to corneal surface under topical anaesthesia
Examiner uses slit lamp or direct ophthalmoscope to review the iridocorneal angle.
Both eyes should be compared if possible.
If one eye too much corneal oedema/active glaucoma which can collapse the drainage angle use the other eye to help identify if likely goniodysgenesis and primary glaucoma as goniodysgenesis almost always a bilateral condition.
129
How is glaucoma classified?
Primary vs Secondary (due to other ocular disease)
130
What are the 2 types of primary glaucoma?
Open angle - drainage angle appears normal on gonioscopy in early stages of condition, occurs sporadically in the UK. Fundamental lesion undetermined but increased resistance to outflow may be due to abnormal glycosaminoglycan build up in the trabecular meshwork.
Closed angle/narrow angle (goniodysgenesis) - pectinate ligament congenitally abnormal
Sheets of tissue containing only small flow holes replace the normal structure of trabecular meshwork.
Span of the pectinate ligament is often reduced also.
In early life these limited channels may allow sufficient passage of aqueous for maintenance of normotensive globe.
Later in life (middle age) the aqueous outflow becomes so compromised that glaucoma then develops.
Closed angle goniodysgenesis most common cause of primary glaucoma in dogs in the UK.
131
What breeds are predisposed to primary open angle glaucoma?
Norwegian Elkhound
Beagles
Petit Basset Griffon Vendeen
132
Which breeds are predisposed to primary closed angle glaucoma (goniodysgenesis)?
English Cocker Spaniel
American Cocker Spaniel
English Springer Spaniel
Welsh Springer Spaniel
Bassett Hound
Bouvier des Flandres
Labrador
Golden Retriever
Flat Coated Retriever
Great Dane
Welsh Terrier
Dandie Dinmont
Shiba Inu
Siberian Husky
Samoyed
Chow Chow
Shar Pei
Boston Terrier
Yorkshire Terrier
Miniature Poodly
Can occur sporadically in any breed or crossbreed dog however.
133
Which ocular problems can lead to secondary glaucoma?
Anterior lens luxation (N.B glaucoma can also lead to lens luxation)
Uveitis - synechiae formation and iris bombe or blockage of the drainage angle with iridial swelling/inflammatory debris
Neoplasia - infiltration of drainage structures, fibrovascular membrane formation or resulting secondary uveitis
Abnormal pigment deposition (ocular melanosis) in the Cairn Terrier
Intraocular haemorrhage - blockage or drainage angle with blood clots
Vitreous prolapse after intraocular surgery
Fibrovascular membrane formation over pectinate ligament - chronic uveitis, retinal detachment and neoplasia.
134
What are the 3 questions you should ask when faced with a glaucoma case?
1. Is this truly glaucoma - tonometry, does it fit (breed), presentation.
2. Primary Vs Secondary glaucoma - gonioscopy (good eye if unable to assess in bad eye) vs presenting pathology
3. Acute or Chronic presentation - (enlarged globe = always chronic as takes week/months to occur, unless puppy/kitten)
135
Describe the gonioscopy grading scheme - how does the grade affect breeding recommendations?
Gonioscopy - looking for pectinate ligament dysgenesis (goniodysgenesis)
Grade 1 = 1-25% abnormal
Grade 2 = 25-75% abnormal
Grade 3 = 75% + abnormal
95-100% = glaucoma
Grade 0-1 = ok for breeding
Grade 2 = amber, look at individual age, progression, repeat score every 3 years, if planning to breed mate with individual with 0 or 1 score
Grade 3 = red, do not breed
136
Describe the clinical signs of acute glaucoma. How should they be prioritised?
Acute glaucoma = emergency, act quickly to reduce pressure and try to save/maintain vision
1. Pain leading to blepharospasm, head shyness and anorexia/depression
2. Episcleral and conjunctival congestion
3. Vision loss in affected eye - absent dazzle, menace, PLR
4. Corneal oedema - 'steamy' cornea especially if IOP >50
5. Mydriasis - dilated pupil poorly responsive to light (caused by iris sphincter muscle paralysis with high IOP)
137
Describe the clinical signs seen with chronic glaucoma. What is the aim of treatment in these globes.
1. Pain reduced from acute phase
2. Globe enlargement - buphthalmos/hydrophthalmos
3. Haab's striae - tears in Descemet's membrane seen as grey streaks in cornea
4. Cupping of optic disc at the lamina cribosa - weak point in sclera where it is penetrated by optic nerve
5. Optic nerve atrophy
6. Retinal degeneration +/- detachment
7. Intraocular haemorrhage seen occasionally
8. Phthisis bulbi - end stage - caused by pressure induced atrophy of ciliary body.
9. BLIND
Vision gone in these eyes and prognosis poor
Aim is to make eye comfortable (often whilst counselling owner about enucleating eye)
Often require enucleation in the long term
138
What should we do about the 'good/non glaucomatous' eye in individuals who are found to have primary glaucoma.
Warn O's likelihood that can develop glaucoma in other eye at some stage - often within 6 months.
Start on prophylactic pressure medication for other eye - carbonic anhydrase inhibitor e.g Cosopt/Trusopt/Azopt
Reduces production of aqueous humour - BID dosing for prophylaxis.
139
How does goniodysgenesis tend to present?
Acute onset unilateral disease - often blind in clinically affected eye by presentation
Middle age generally but can be younger.
Other eye is also affected as goniodygenesis bilateral but not clinical at this stage - start prophylactic carbonic anhydrase inhibitors.
140
How does primary open angle glaucoma tend to present?
Tends to be bilateral in presentation and onset is gradual.
Globe enlargement and lens subluxation often visible at first presentation.
Even severely enlarged globes with primary open angle glaucoma can remain sighted for extended periods of time.
141
List the ddx for the following signs often seen with glaucoma:
Pain
Corneal Oedema
Mydriasis
Episcleral congestion
Corneal vascularisation/pigmentation
Lens Luxation
Intraocular haemorrhage
Enlarged globe
Blindness
Pain = corneal ulceration, uveitis, foreign body, retrobulbar cellulitis/abscess
Corneal oedema = corneal ulceration, uveitis, endothelial degeneration/dystrophy, lens luxation
Mydriasis = iatrogenic (atropine), iris atrophy (post uveitis/senile), anxiety, dim room light/pen torch, blindness and associated causes, anxiety.
Episcleral congestion = uveitis, episcleritis, retrobulbar space occupying lesion, panophthalmitis
Corneal vascularisation/pigmentation - KCS, uveitis, pannus (CSK), keratoconjunctivitis, post ulceration, exposure keratopathy, trichiasis
Lens luxation = primary lens luxation (terriers/border collies)
Intraocular haemorrhage = trauma, hypertension,
intraocular neoplasia, uveitis, coagulopathy, collie eye anomaly, retinal dysplasia, persistent hyperplastic primary vitreous
Enlarged globe = may appear enlarged at first glance with retrobulbar space occupying lesion (TEL also protrudes if mass extraconal)
Blindness = severe corneal disease, uveitis, optic neuritis, SARDs, retinal detachment, progressive retinal atrophy, blindness of CNS origin.
142
What mechanisms do we have to reduce the pressure using medications in glaucoma?
Need to decrease pressure
Can do this either by reducing AH production (carbonic anhydrase inhibitors)
OR
Increasing rate of drainage of AH (prostaglandin analogues)
143
What is the prognosis for glaucoma generally?
Overall prognosis for vision in most cases of glaucoma = poor
Many cases blind within few hours or days of a high IOP
Best chance of success is to identify and treat early (often however not presented to us until chronic stages or after several hours to days of being glaucomatous - substantial irreversible change has occurred to the outflow system by this stage)
144
When can IOP curves be used?
Glaucoma - assessing response to medical therapy
Patient admitted and IOP readings recorded intermittently (every few hours) - assesses response to medication and frequency of dosing required.
145
What options do we have for medical management in glaucoma cases?
Hyperosmotic agents (Mannitol/Glycerol) - acute glaucoma only
Aqueocentesis - acute glaucoma only
Prostaglandin analogues (Latanoprost/travoprost)
Carbonic anhydrase inhibitors (Dorzolamide/Brinzolamide
Beta blockers (often combination product e.g Cosopt = brinzolamide/timolol)
146
How do hyperosmotic agents work for glaucoma treatment? Why are they generally not used as first line therapy anymore?
Mannitol (10 or 20% solution 1 to 2g IV over 30 mins)
Glycerol (50% given orally at 1-2ml/kg, less effective than mannitol and may induce vomiting)
Leads to osmotic diuresis - diffusion of water from aqueous and vitreous into plasma leading to reduced IOP.
IOP usually reduced within 1hr and effect can last up to 24hrs (mannitol), 10hrs (glycerol)
Potential side effects - dehydration, care in patients with renal/cardiac compromise, nausea and vomiting, hyperglycaemia and glycosuria (rapidly metabolised to glucose)
Contraindicated in diabetic patients.
147
What is the first line preferred treatment for glaucoma in dogs. When is this type of drug contraindicated however?
Why does this drug not work in cats?
Prostaglandin analogues - Latanoprost/Travoprost
Interact with prostaglandin FP receptors - increase outflow by uveoscleral outflow (non conventional) pathway
Contraindicated - anterior lens luxation (causes miosis worsening pupil block), severe uveitis (may worsen - therefore not usually used for secondary cases of uveitis)
Good at significantly reducing IOP rapidly
Applied at least BID but often more than this required
Inefficient in cats - lack prostaglandin F (FP) receptors in uveal tract and trabecular meshwork (have EP receptors instead)
148
How do carbonic anhydrase inhibitors work against glaucoma? When may they be used?
CAI's = decreased AH production
Dorzolamide and Brinzolamide
Prevent formation of bicarbonate ions in ciliary epithelium
(Rarely used systemically due to s/e = metabolic acidosis, hypokalaemia, anorexia, vomiting, diarrhoea)
Rarely efficient enough to control IOP in cases of primary glaucoma but can be used for secondary glaucoma and prophylactically for other eye.
3x daily application
Cats = only evidence for efficacy of trusopt (dorzolamide), brinzolamide has no effect on normal IOP of cats but does reduce IOP in dogs.
149
When may beta antagonists/beta blockers be used in glaucoma? What side effects are associated with their use?
Combination products (Cosopt = brinzolamide/timolol) or on own timolol.
May be slightly more efficient than just CAI on own at reducing moderate pressure elevations.
B blockers on own often uneffective in canine glaucoma.
Possible side effects - bradycardia, hypotension
150
When may a cholinergic agonists be used in glaucoma management?
Pilocarpine
Parasympathomimetic
May be used in primary open angle glaucomas in dogs
1% just as effective as other formulations - applied 2-3x daily
Should not be used with uveitis or luxated lens due to s/e of disruption to blood-aqueous barrier and miosis.
151
How should we approach treatment of glaucoma secondary to uveitis? What is the one scenario with glaucoma where we may want to apply atropine and what other drug may help in this situation?
Aggressive medical therapy addressed at uveitis - vital early on in course of disease
Topical and systemic steroids indicated.
Iris bombe may develop due to 360 posterior synechiae - atropine can be applied in this one scenario with glaucoma
10% phenylephrine may also be used to encourage mydriasis and breakdown of adhesions.
152
When may a lendectomy be performed?
Intracapsular lendectomy may be required in cases of glaucoma secondary to primary anterior lens luxation.
Jack Russell Terriers, Parson Terrier, Wire Haired Fox Terriers, Miniature Bull Terrier and Tibetan Terriers predisposed to PLL as well as Lancanshire Heelers, Borders Collies and Shar Peis.
(Beware glaucoma can cause lens luxation and some terriers can get primary glaucoma as well as being predisposed to lens luxation - in these cased lendectomy alone unlikely to solve the issue)
Even if primary lens luxation has caused glaucoma removal of the lens may not resolve the glaucoma and some dogs may require lifelong medical management post operatively.
153
What types of surgery may be performed for the treatment of glaucoma?
By-pass surgery (alternative outflow channel for aqueous)
1. Scleral trephination with peripheral iridectomy is simplest bypass technique but had potential for serious complications and tends to fail within few weeks or months (if not immediately post op)
2. Drainage implant surgery = better results in medium term but is expensive +++ and outcomes vary - enters anterior chamber at limbus and is retained under the rectus muscles covered by conjunctiva.
Both procedures often fail in long term due to development of fibrosis around the region of the site of aqueous absorption and drainage. The use of (toxic) fibroblast agents may reduce this complication but often causes other problems.
Procedures to reduce aqueous formation:
1. Laser cyclophotocoagulation = technique of choice
Can be used on eyes with vision but causes post op IOP spike which needs to be treated (aqueocentesis often used for this) to prevent further vision loss. Often causes post op inflammation (intraocular fibrin formation/uveitis/haemorrhage) which needs to be controlled
Can also cause corneal ulceration, keratoconjunctivitis, cataract formation and if drop too excessive pthisis bulbi.
Trans-scleral diode laser.
Endoscopic version has also been advocated and has superior long term success rates BUT need to remove lens for access to ciliary body intra-operatively and no peer reviewed data.
2. Cyclocryotherapy - may be used in blind eyes to reduce the pressure, risk of retinal detachment as well as IOP spikes. Best avoided in sighted eyes.
Cryoprobe placed over ciliary body behind limbus and frozen in several places until ice ball extends into limbus.
IOP often increased for several days after.
3. Intravitreal gentamicin - used to ablate the ciliary body
Can cause chronic uveitis and pain so rarely used.
Cannot be used in cats
Should not be used where evidence of neoplasia, infection or uveitis.
Eye irreversibly blind - should not be used in sighted eyes.
IN BLIND, PAINFUL EYES ENUCLEATION IS OFTEN THE BEST OPTION - predictable, permanent resolution and economical results.
ALTERNATIVE = EVISCERATION AND PLACEMENT OF INTRASCLERAL PROSTHESIS - can be acceptable alternative for clients who are unable to accept their pet losing an eye cosmetically (or potentially both eyes if affected by primary glaucoma).
Ethics? - persistent corneal ulceration and KCS - only cosmetic.
154
What type of glaucoma is most common in cats?
Secondary glaucoma (often following on from uveitis or intraocular neoplasia)
Often presents late on in the disease process as more subtle.
Anisocoria/buphthalmos often the most common ways O's detect glaucoma.
155
Which breeds of cat may be predisposed to primary glaucoma?
Siamese, Persian, Burmese
Closed angle is seldom, if ever recognised in cats
Open angle described in the above breeds as well as sporadically in DSH and long haired cats.
Some cases - myxomatous change in blood vessels associated with AH outflow (scleral venous plexus and vortex veins)
156
What is aqueous misdirection syndrome in cats?
May result in secondary glaucoma in some older cats
AH flows directly into vitreous resulting in anterior displacement of the vitreal face, lens and iris
These cases present with very shallow anterior chamber- glaucoma develops due to reduced aqueous humour outflow through compromised drainage angle.
These cases may be managed surgically with lendectomy by phacoemulsification combined with vitrectomy.
157
How does lens luxation usually occur in the cat?
Lens luxation in cat is always secondary to chronic anterior uveitis or globe enlargement (rarely trauma).
Less likely to get high pressures compared to dogs - shape of pupil is slit, not as blocked by the lens
Often can leave as long as pressures not raised (normally not)
Not seen often as cause of glaucoma in the cat.
158
How does glaucoma generally tend to present in cats.
Insidious - gradual onset
Less obvious ocular pain, corneal oedema, episcleral/conjunctival congestion compared to dogs
More commonly change in appearance of pupil or globe becoming enlarged are first signs noted by owners.
For this reason cases with chronic uveitis require ongoing IOP monitoring especially given that topical and even systemic corticosteroids may raise IOP in cats.
159
Why is treatment of glaucoma in cats often unrewarding?
1. Cats typically present later on in disease process
2. Glaucoma usually secondary to something else
3. Effective drugs for feline glaucoma are limited.
160
What is the main aim of treating feline glaucoma?
What drugs may we use in feline glaucoma?
Address underlying cause!
Feline glaucoma - prostaglandin analogues e.g latanoprost ineffective for IOP (may still cause miosis)
Dorzolamide (topical carbonic anhydrase inhibitor) - 3-4x daily
(Brinzolamide no effect on IOP of normal cats in studies)
?Cosopt - dorzolamide/timolol - reduces IOP in normal feline eyes but efficacy remains undetermined in glaucoma.
Ultimately if globe painful, blind and persistently elevated pressure of >40mmHg and/or ulcerative keratitis (due to associated lagophthalmos) then enucleation should be considered.
161
Why are cats with glaucoma not candidates for evisceration/intrascleral prosthesis placement unlike dogs?
Risk of developing post traumatic sarcoma in future
