The Fundus Flashcards

Question

What are the 4 portions of the optic nerve (CN II) and what does the optic nerve consist of?

Answer 1

Intraocular Intraorbital Intracanicular Intracranial Optic nerve consists of ganglion cells axons surrounded by myelin.

Answer 2

Axoplasmatic flow = important for optic nerve function and metabolism but pressure sensitive >50mmHG = no flow

Answer 3

Location where retinal ganglion cells turn approximately 90 degrees to exit the eye as the optic nerve. Located ventrolateral to posterior pole of eye and remains fixed due to the underlying optic foramen.

Answer 4

Presence of myelin and degree of myelination (cats = occurs posterior to the disc making it appear round and dark whereas dogs = myelination typically begins at the disc leading to variations in size, shape and colour based on the myelination extent) Visibility may vary based on tapetal and non tapetal regions, appearing in either the tapetal fundus, non tapetal fundus or at their junction.

Answer 5

Centre of the disc may show a dark spot Represents the origin of the embryonic hyaloid vasculature Particularly prominent in myelinated optic nerve heads Rarely some residual hyaloid tissue may remain and extend short way into the vitreous (Bergmeister's papilla)

Answer 6

Complex gel Mainly water (99%) Collagen fibres that form structural framework~ Hyaluronic acid - cells hyalocytes Mucopolysaccharides Role = maintain ocular shape and volume Keep structures such as lens and retina in proper positions Small role in nutrition for the posterior lens and retina Refractive index similar to lens does not contribute significantly to light refraction (but must remain transparent to allow light to pass through) Storage site for retinal metabolites and waste products - e.g glycogen, potassium, free radicals and lactate.

Answer 7

Scotopic vision (very low light intensities) - only rods are active Mesopic vision (medium light intensities) - both rods and cones active Photopic vision (bright light intensities) - rods are oversaturated and only cones continue to function In ERG the function of the rod and cone photoreceptors can be distinguished using different light intensities during retinal stimulation.

Answer 8

Determined by photopigment classes in the CONE retinal photoreceptors. Classified by the wavelength at which the OPSIN molecule in the cone photoreceptors has its peak absorption.

Answer 9

Humans & Primate = trichromatic vision Possess blue, red and green OPSIN Dogs & Cats dichromatic (deuteranope) - blue opsin and red opsin Horse dichromatic (protanope) = blue opsin & green opsin Reptile, fish, avians - tetrachromatic (additional opsin molecule with peak absorbance in UV range)

Answer 10

Visual acuity = high resolution vision and visual discrimination Cones > Rods Cones and their retinal ganglion cells have high density in the central retina - this is known as the area centralis/visual steak (although in dogs/cats and horses rods still outnumber cones accounting for lower visual resolution and greater light sensitivity) Birds = fovea instead, only populated by cones and provides high visual acuity and colour perception.

Answer 11

Enhances vision in low light settings but decreases visual acuity through light scatter.

Answer 12

Rods = motion Rod rich retina in most domestic mammals - motion detecting ability especially in low light is well developed.

Answer 13

Examine fundus after dilation so can visualise peripheral fundus (unless glaucoma/lens instability prevents) - topical 1% tropicamide Methods to examine the fundus: Indirect ophthalmoscopy - monocular (20D and 30D lens) and binocular techniques (head mounted) Inverted and reversed virtual image, wide field view of fundus - identify lesions Distant direct ophthalmoscopy - tapetal reflection assessment Close direct ophthalmoscopy - magnified view of area of fundus 'zoom in' on areas on interest identified with the indirect method. Upright image with 15-17x magnification,

Answer 14

Indirect = broad field of view, reduced magnification (better for overall assessment of the fundus, maintain greater working distance from patient - good if temperament not very amenable!) Binocular indirect has benefit of stereopsis - 3D perception of depth in the observed structures Disadvantage = image INVERTED AND REVERSED (upside down and backwards) and virtual. Close direct = examine areas in greater magnification 15-17x, 'zoom in' on areas identified on indirect exam, true image Both techniques complement each other and should be performed together when examining the fundus.

Answer 15

ERG = technique that measures small electrical potentials generated in the retina when it is stimulated by light. Potentials known as 'waves' are recorded using a corneal electrode and amplification and recording systems. ERG = assessment of retinal function Indications for use: Retinal function in cataract patients prior to surgery Differentiate causes of sudden blindness where retinal lesions are not visible (SARDS, early retinal degeneration/PRA, optic neuritis without papillitis, CNS disease)

Answer 16

ERG responses will vary based on factors such as: Dark adaptation & Light stimulus characteristics Use these responses to isolate rods/cones Dark adapted conditions - dim light stimulus primarily elicits response driven by rods Light adapted conditions - response mainly driven by the cones Pure cone driven response to flickering light stimuli at 30Hz or higher

Answer 17

Sedated patient Recording system Amplification Electrodes - jet corneal contact lens, subdermal reference and earthing electrode) Flash photo stimulator Farraday cage - prevent intereference

Answer 18

A wave = photoreceptor response B wave = bipolar cells C wave = retinal pigment epithelium Flatline on an ERG = peripheral blindness

Answer 19

Differences in anaesthetic protocol Temperature Oxygenation Farraday cage use = less interference from other electrical equipment Species Breed Age Try to standardise protocols for ERG's as much as possible to help with interpretation.

Answer 20

Ocular ultrasound Pathology can see affecting fundus: Persistent embryological structures in vitreous Intraocular neoplasia Retinal detachments (highly reflective, continuous linear structure with attachments at optic disc posteriorly and ora ciliaris anteriorly resembling wings of a seagull)

Answer 21

MRI (Ultrasound can be used but difficult and much less sensitive)

Answer 22

Red/blue chromatic pupillary light reflex - used to distinguish between outer and inner retina as well as optic nerve disease in canine patients. Evaluates PLR in response to red or blue light. Red light = stimulates both rods and cones due to its high intensity Blue light = activate melanopsin in specific ganglion cells as well as rods and cones Blue light can therefore trigger PLR response independently of the photoreceptors. Photoreceptor degeneration - red PLR absent but blue PLR intact due to intact retinal ganglion cells SARDS = most common indication With SARDS blue PLR remains intact whilst red PLR absent (photoreceptor loss) Optic neuritis = both PLR reflexes lost 75% sensitivity and 100% specificity in detecting retinal degeneration and detachment - swift, easy and accurate diagnostic tool for canine patients with retinal and optic nerve disease.

Answer 23

DNA testing Eye examinations The two should be used complementarily

Answer 24

Eye examination scheme - BVA, performed by ophthalmologists selected to be on their panel Used to detect clinical signs of neonatal/congenital hereditary eye disease Litters of puppies and breeding dogs should be examined under the scheme (ideally annually) Final examination when the dog is 8yrs also recommended to ensure late onset inherited diseases are recorded accurately. Eye examination = identification of phenotype (physical presence of disease) Eyes examined thoroughly with slit lamp, indirect and direct ophthalmoscopy and additional gonioscopy in some breeds affecting by pectinate ligament abnormality/goniodysgenesis.

Answer 25

DNA screening - identification of genotype Simple = often cheek swab 2 types = mutation detection tests and linkage tests Mutation - precisely identify specific mutated gene causing the disease, categorising animals as genetically clear, carriers or affected for recessively inherited conditions. Linkage - only identify approximate location of the mutation, not the actual mutation itself making them less accurate than mutation tests. Advantages = can be conducted on animals of any age (before breeding and sexual maturity - some diseases do not present clinically until much later in animals life when has already been bred from), detect carriers who are not clinically affected but in breeding could lead to affected individuals in recessive conditions. Identification of actual mutation - 100% accurate with no subjectivity (linkage tests do carry margin of error) Disadvantage - need to know the specific mutation for the disease in order to perform DNA testing

Answer 26

Genetic DNA testing = 100% accurate (excluding sampling/lab error), only tests for a single specific gene mutation, identifies carriers for recessive diseases, identifies genetically clear animals for breeding, identifies animals before onset of clinical signs of eye disease (several inherited eye diseases do not present until later in life when animal has already been bred from) - GENOTYPE Need to know specific gene mutation for this to be used however - many inherited eye diseases unknown gene for inheritance. Eye examination = more subjective interpretation, screens for wide range of both inherited and non inherited ocular disease, unable to identify carriers, cannot distinguish unaffected from carrier animals and those animal affected with late onset disease prior to breeding, unable to identify affected animals until ocular clinical signs become apparent. - PHENOTYPE

Answer 27

Congenital inherited condition During embryonic development lens receives nutrients from hyaloid artery which reaches the posterior lens around day 25 of gestation. Tunica vasculosa lentis also develops around this time. Day 45 vascular supply should start to regress as well as the primary vitreous and this process should be fully completed by 2-4 weeks post birth. In some cases there is persistence of these vessels and this leads to formation of fibrovascular plaques on the posterior lens capsule. Plaques = yellow/white densities, pigment foci and visible blood vessels Often associated with lens colobomas, persistent capsulopupillary vessels, posterior lenticonus, intralenticular and retrolental haemorrhage, secondary cataracts and persistence of hyaloid artery. Breeds predisposed = Dobermann, Staffordshire Bull Terrier Inheritence complex - suspect autosomal dominant with incomplete penetrance Specific genes not identified. Grading scheme depending on severity of lesion. High grades may affect vision.

Answer 28

Term that encompasses various congenital and neonatal conditions where the retina has abnormally differentiated during embryonic development. Genetic (majority) vs external factors (e.g radiation, infectious agents e.g canine herpes virus)

Answer 29

Most cases of inherited retinal dysplasia caused by autosomal recessive gene defects.

Answer 30

Multifocal retinal dysplasia vs Total retinal dysplasia Multifocal = vision normal in many dogs Total = blindness

Answer 31

Linear folding of the sensory retina (photoreceptors curled up on histopathology) and formation of rosettes comprised of neuroretinal cells. Range of lesions = vermiform (worm like) grey streaks, dots and circles to tapetal hyperreflectivity sites with or without hypertrophy of the retinal pigment epithelium.

Answer 32

Linear folding of the sensory retina with formation of rosettes of neuronal retinal layers surrounding a central lumen. Often hypertrophy of the surrounding retinal epithelium with increased pigment.

Answer 33

Geographic retinal dysplasia = subtype of multifocal retinal dysplasia Circular areas of dysplastic retina Commonly observed dorsal to optic disc in tapetal fundus

Answer 34

Retinal dysplasia = congenital Not usually progressive Can be remodelling over time so lesions become less obvious (especially smaller folds) In other cases can become more demarcated with increased pigment deposition and hyperreflectivity.

Answer 35

Congenital - look for this disease in puppies 6-8 weeks before being sold (however geographic form rarely detected in dogs less than 9 weeks) Current recommendation = screen at 6-9 weeks then again at 6-12 months before breeding.

Answer 36

English Springer Spaniel Cavalier King Charles Spaniel Hungarian Pulis Rottweilers Golden Retreivers American Cocker Spaniels

Answer 37

More complex type of retinal dysplasia Associated with complete detachment or non attachment of areas of the retina Non attachment = due to failure of contact between the inner and outer layers of the optic cup during embryogenesis. Dogs with this form of retinal dysplasia often blind Other ocular abnormalities = microphthalmos, cataracts, nystagmus

Answer 38

Bedlington Terriers Labrador Retrievers Sealyham Terriers Yorkshire Terriers Samoyed Labradors and Samoyed TRD can also be associated with ocular skeletal dysplasia with severe ocular defects and short limb dwarfism.

Answer 39

Irradiation Infecition in utero - canine herpesvirus or adenovirus Vitamin A deficiency

Answer 40

Congenital disorder (complex) affecting retinal, choroidal and scleral development Bilateral disease but not usually symmetrical in presentation.

Answer 41

Choroidal hypoplasia (CH) = hallmark Typically seen in lateral or dorsolateral region of the fundus near the optic disc Affected area = pale patch due to localised lack of retinal and choroidal pigment + tapetum Choroidal vessels in the area may show abnormalities in size, number and disposition.

Answer 42

Choroidal hypoplasia - visible and detectable on fundus examination between 6-7 weeks of age but can be masked in as many as 50-60% of affected animals by development of pigmentation in the fundus Eye examination for affected breeds recommended at 5-6 weeks of age Litter screening + DNA testing is the most effective approach for screening for this disease.

Answer 43

Rough Collie Smooth Collie Shetland Sheepdog Lancashire Heeler Border Collie Bearded Collie Australian Sheepdog Kelpie

Answer 44

Optic nerve head colobomas +/- colobomas of adjacent tissue Lesions are seen as depressions or holes Present in up to 30% of dogs with CEA Choroidal hypoplasia = does not usually impact vision Optic nerve head colobomas = visual impairment and retinal detachment, possibly intraocular haemorrhages although rare.

Answer 45

Optic nerve aplasia (very rare) - complete lack of optic nerve, also often lack retinal vasculature and may show other congenital abnormalties such as microphthalmos, retinal disorganisation and anterior segment dysgenesis. Ocular nerve hypoplasia and micropapilla - very small optic disc dimension, Visual deficits from near normal vision to total blindness dependent on severity of hypoplasia Micropapilla = incidental finding unless clinical signs Both hypoplasia and micropapilla = small and relatively grey optic discs due to lack of myelinated fibres visible on disc surface May occur sporadically in various dog breeds either alone or accompanying other ocular malformations.

Answer 46

Congenital malformation of the optic nerve head Outward distortion of the ONH due to focal absence of normal tissue in the ONH and/or peripapillary sclera. Most commonly assciated with choroidal hypoplasia as part of CEA Can also occur sporadically alone or with other ocular defects. Breeds - Basenjis, Dachshunds, Old English Sheepdogs Small colobomas - generally little effect on vision, larger colobomas that communicate with vitreous and subretinal space - risk of retinal tears, detachments and blindness. Also risk of haemorrhage due to neovascularisation of the retina.

Answer 47

PRA = progressive retinal atrophy Group of inherited retinal diseases - affects various canine breeds Characterised by the degeneration of the photoreceptor cells in the retina (rods and cones) 2 main types - developmental and degenerative Developmental/Dysplasia = early onset and affects the normal development of photoreceptors leading to rapid vision loss - as early onset as 2 months Degenerative = involves normally developed photoreceptors, onset and progression to loss of vision = slower, affected animals often several years of age.

Answer 48

Initial night blindness (nyctalopia) due to loss of rod photoreceptor function Progresses to vision loss under all forms of lighting Poor PLR reflexes Persistently dilated pupils Ophthalmoscopic exam = generalised, bilateral increase in reflectivity of the tapetum (tapetal hyperreflectivity) due to progressive retinal thinning As disease advances also see narrower retinal blood vessels (becoming barely visible) and optic disc becomes paler due to atrophy. Non tapetal region of fundus shows depigmentation as the disease progresses Cataracts and retinal detachments can be seen associated with PRA.

Answer 49

PRCD - Progressive Rod-Cone Degeneration Affects over 30 breeds Autosomal recessive inheritance.

Answer 50

History - vision changes (progressive nature, often started as night blindness) Ophthalmoscopic findings - bilateral mydriasis, hyperreflective tapetum, pale optic nerve head, attenuated retinal vasculature, depigmentation of non tapetal fundus (Caution as some non inherited retinal degenerations can mimic the appearance of PRA) DNA based tests for certain breeds can be used to confirm the presence of the gene mutations known to cause PRA. Some breeds may have more than 1 type of PRA however so may need to submit several tests. ERG and Chromatic Pupillary Light Reflex - can be used to assess retinal function ERG - can detect photoreceptor changes at early stage - reduced to absent rod mediated ERG responses. Chromatic PLR - can be used to indicate photoreceptor function. Completely absent to reduced red light response (due to loss of photoreceptors), slight reduced blue light response in earlier stages (still functioning retinal ganglion cells), late stages - complete loss of blue light response as well.

Answer 51

Usually classified and named based on affected cell type PRCD - Rod-Cone degeneration (most common) CRD - Cone - Rod CD - cones only Different genes involved all with similar clinical presentation Due to genetic mutations in enzymes of the phototransduction process, leads to accumulation of substrates and photoreceptor cell death.

Answer 52

No treatment for PRA - often dogs learn to cope with blindness Prevention - DNA testing prior to breeding + eye examinations under Eye Examination scheme in at risk breeds Usually autosomal recessive - DNA tests can help identify carriers and prevent breedings of carriers to carriers. Autosomal dominant and X linked types seen less frequently.

Answer 53

Australian Cattle Dog Rough Collie Dachshund (Miniature Long Hair) Gordon Setter Irish Setter Irish Wolfhound Miniature Schnauzer Papillon Lhaso Apso Norweigian Elkhound Miniature and Toy Poodle Chesapeake Bay Retriever Golden Retriever Labrador Retriever Nova Scotia Duck Tolling Retriever American Cocker Spaniel Cocker Spaniel English Springer Spaniel Tibetan Spaniel Tibetan Terrier Welsh Corgi

Answer 54

Day blindness Specific form of PRA CONE DISORDER ONLY - impaired day vision from early age but night vision is unaffected Non progressive generally Alaskan Malamute, Gordon Setter, Labrador Retriever, German Shorthaired Pointers and Miniature Australian Shepherds reported to be affected. Mutations in CNGA3 and CNGB3 genes responsible Ophthalmoscopic exam = no abnormalities ERG = diagnosis Lack of cone function

Answer 55

RPED - progressive retinal atrophy that only affects outermost layer of retina the retinal pigment epithelium. Deficiency in the RPE ability to degrade used photoreceptor material - accumulation of LIPOPIGMENT in their cytoplasm. Very rarely causes blindness but can cause visual deficits in advanced stages - difficulty seeing stationary objects. Only affects tapetal fundus, sparing peripheral vision due to the protective effect of the melanin in the non tapetal fundus. Ophthalmoscopic findings = tapetal fundus irregular light brown spots, gradual increase in size and become more wide. Hyper-reflectivity and atrophic changes around pigment foci indicating retinal atrophy As progresses lesions coalesce into irregular patches with hyperreflective areas in the tapetal fundus. Breeds -Border Collies, Briards, Rough Collies, Smooth Collies, Golden Retrievers, Labrador, Shetland Sheepdogs, Cocker Spaniels, Springer Spaniels and Corgi's. RPED ASSOCIATED WITH VITAMIN E DEFICIENCY IN ENGLISH COCKER SPANIELS - similar retinal lesions and neurologic dysfunction. Blood test to determine alpha-tocopherol levels Supplementation with high levels of dietary vitamin E can improve neurologic signs in affected dogs but ophthalmic lesions will remain. (Ataxia and Paresis most common neurological signs)

Answer 56

Hereditary retinal dystrophy Mutation in RPE65 gene - defect in retinal polyunsaturated fatty acid Congenital night blindness in affected dogs Progressive - leads to day vision blindness also in advanced cases Experimental gene therapy - subretinal injections of RPE65 gene

Answer 57

Hereditary condition - development of multiple retinal bullae Young dogs 3-6 months - no progression beyond 1 year Results from secretion and absorption defects in the RPE (type of dysplasia) Recessive inheritance Mutations in BEST1 gene - other mutations cmr1, cmr2 and cm3 Breeds - Great Pyrenees, Coton du Tulear, Mastiff, Bullmastiff, Finnish Lupphund, Lapponian Herder Multifocal grey-tan retinal detachments in affected dogs - mostly peripheral tapetal fundus and around optic nerve head. Occasional beneath major veins. Peripapillary lesions develop quickly, peripheral more slowly. Over time detachments may regress, remain stable or progress into areas of multifocal retinal degeneration but do not progress beyond 1 yr of age.

Answer 58

Congenital: Collie Eye Anomaly Optic nerve coloboma Optic nerve aplasia/hypoplasia/micropapilla Retinal dysplasia = multifocal (MRD) including geographic MRD vs total (TRD) Inherited: PRA (many forms) RPED Retinal dystrophy (Briards) Canine multifocal retinopathy

Answer 59

Early onset rod-cone dysplasia Late onset rod-cone degeneration

Answer 60

Breeds - Persians, Bengals, Abyssinians Dominant inheritance reported in Abyssinians Mutation in CRX gene in Abyssinians and AIPL1 gene in Persians Affected kittens = mydriasis, nystagmus and impairment of PLR Ophthalmoscopic findings - signs of retinal degeneration as early at 8-12 weeks ERG = early loss of rods and scotopic function As disease progresses affects cones as well By age of 1 year most cats are blind.

Answer 61

Abyssinians = most affected Recessively inherited Signs appear 1.5-2yrs of age Progress to complete atrophy by 4-6 years Ophthalmoscopic findings and clinical signs similar to that described for PRA in dogs. Hyper-reflective tapetum Lack of retinal vasculature Depigmentation of non tapetal fundus Dark and atrophied optic nerve head.

Answer 62

Close proximity of both of these structures Often breakdown of the blood-retinal barrier with inflammation Choroid = part of uvea therefore chorioretinitis can often be referred to as posterior uveitis.

Answer 63

SYSTEMIC INFECTIONS Chorioretinitis should be regarded as an ocular manifestation of systemic disease rather than a primary ocular disease.

Answer 64

Varying signs depending on degree and severity of inflammation and whether active. Active signs of chorioretinitis: 1. Perivascular cuffing - grey-white opacities caused by accumulation of inflammatory cells around blood vessels 2. Retinal oedema - greyish hyporeflective lesions resulting from fluid accumulation, dull tapetum in these areas 3. Haemorrhage 4. Detachment of the neurosensory retina 5. Granulomatous lesions 6. Vitreal haze/synersis - clouding and liquefaction of the vitreous

Answer 65

1. Chorioretinal scars - tapetum shows areas of hyperreflectivity and the centre of the lesion becomes pigmented due to pigment proliferation in the RPE 2. Non tapetal fundus - areas of depigmentation (mottled appearance), pigment clumping and exposure of choroidal vessels/sclera becomes visible. May be atrophy of choroidal vessels in this region also.

Answer 66

SYSTEMIC CAUSE- unable to diagnose aetiology on ocular examination alone Always look for systemic cause even when no other obvious systemic signs. 1. Full physical examination 2. Haematology, Biochemistry and Urinalysis - evidence of infectious, vascular or renal disease. (Infectious disease testing if indicated) 3. Systolic blood pressure measurement 4. Ultrasonography of abdomen 5. Radiography/CT of thorax 6. FNA of any lesions 7. Centesis of aqueous humour (vitreous/subretinal) for cytological or serological evaluation

Answer 67

Infectious disease - viral, bacterial, parasitic, protazoal, rickettsial, fungal, algral Inflammatory disease elsewhere in body Immune mediated disease Cardiovascular disease - systemic hypertension, hyperviscosity syndrome, thrombocytopaenia, polycythaemia Neoplasia - multiple myeloma, lymphoma, systemic histiocytosis

Answer 68

Diagnose and treat primary cause! Topical medications cannot reach posterior segment in effective concentrations. SYSTEMIC drugs required. Primary infectious agent doesn't always directly enter the eye but inflammation of choroid and retina occurs due to sensitised immunocytes and antibody production. Systemic anti-inflammatory drugs required to address inflammation in the posterior segment + cycloplegic agents unles patients systemic or ocular condition prohibits their use. Anti-inflammatory choice: Possible infectious aetiology - systemic NSAID Immune mediated/non infectious aetiology - systemic steroids Cycloplegic agent to reduce ciliary spasm = e.g atropine

Answer 69

Viral - distemper Bacterial - Lyme disease (Borrelia), Bartonellosis, Brucellosis Protozoal - Toxplasmosis, Leishmania, Neosporosis Parasitic - Toxocara cania, angiostrongylus vasorum Rickettsial - Ehrlichia, Rocky Mountain spotted fever (Rickettsia) Fungal - Blastomycosis, Cryptococcus, Histoplasmosis, opportunistic deep mycosis (aspergillosis) Algeal - Prototheca

Answer 70

Viral - FIV, FeLV, FIP Bacterial - Tuberculosis (mycobacterium), bartonellosis Protozoal - Toxoplasmosis, Leishmania Parasitic - Toxocara cati Fungal - Blastomycoses, Crytococcus, Coccidomycosis, Candidiasis, Histoplasmosis.

Answer 71

Retinal detachment is characterised by the separation of the neuroretina from the underlying retinal pigment epithelium (RPE) Loss of structural integrity leads to loss of function in the affected areas and can then result in secondary retinal degeneration.

Answer 72

1. Rhegmatogenous detachment - most common type Caused by hole or tear in neuroretina - retinal defect allows vitreous and fluid to dissect the neuroretina from the RPE in the subretinal space exacerbating the condition. Retinal tears and hole expose the RPE and tapetum leading to hyperreflectivity and clear dark appearance of the RPE throught the retinal defect. With dialysis and disinsertion the retina tears in the periphery leading to folds hanging from the optic nerve head - VEIL APPEARANCE Floating veil can be seen behind the lens without the use of an ophthalmoscope 2. Traction detachment - occurs when force from the vitreous body pulls the neuroretina anteriorly Can be due to haemorrhage in the vitreous body or traction bands in the vitreous following a posterior uveitis. 3. Exudative detachment - In exudative detachments fluid and cells are deposited in the subretinal space elevating the neuroretina away from the RPE. Potential infectious and systemic causes should always be ruled out with this type of detachment. Tapetum and RPE look dull and hyporeflective due to the accumulation of fluid/cells in anterior to the RPE and tapetum CAN BE CORTICOSTEROID RESPONSIVE Vitreal haemorrhages may prolong the time for reattachment. In summary: Rhegmatogenous = neuoretina loses peripheral attachments Traction = neuroretina gets pulled anteriorly by vitreous Exudative = neuroretins pushed away from RPE by fluid/cells

Answer 73

Seagull sign - detached retina fixed to posterior wall of the eye at the optic nerve head and the ora serrata. Contrast medium can sometimes help to identify small detachments.

Answer 74

Can vary - from flat, attenuated to normal depending on the extent and duration of the retinal detachment

Answer 75

Congenital - Collie eye anomaly, retinal dysplasia (rhegmatogenous) Lenticular disease - lens luxation, cataract, cataract surgery Panuveitis - inflammation of all layers of the uvea including the choroid, ciliary body and iris Infectious disease (as for chorioretinitis) Cardiovascular diseases - systemic hypertension, hyperviscosity syndrome, thrombocytopaenia, polycythaemia Neoplasia - multiple myeloma, systemic histiocytosis, lymphoma Immune mediated diseases Trauma (often blunt force) Glaucoma Dogs = immune mediated/cataract surgery = most common reason for detachments Cats = systemic hypertension and infectious disease most common reason for detachments

Answer 76

Early detachment - photoreceptors can survive for a limited amount of time by recieving oxygen and nutrients from the choroid through the subretinal space or from the inner retinal vessels across the retina As time goes on however not able to sustain photoreceptors sufficiently and will lead to photoreceptor death - pupils become wide and dilated.

Answer 77

Focus on finding underlying reason for detachment. If ocular causes excluded - CEA, retinal dysplasia, ocular trauma, glaucoma, lenticular disease, panuveitis etc then look for systemic cause. Systemic work up = haematology, biochemistry, urinalysis, blood pressure, infectious disease testing, abdominal imaging +/- thoracic imaging, sampling of any lesions (e.g FNA)

Answer 78

Sudden vision loss through detachment - do have chance of vision restoration through medical therapy or surgery if detected early enough. Photoreceptors survive for approx 1 month receiving oxygen and nutrients via the choroid through subretinal space or inner retinal vessels - time to try and restore vision if caught early enough. Medical treatment - address underlying cause e.g hypertension - start anti-hypertensive medication (amlodipine in cats) Antimicrobial therapy if bacterial infection Anti-inflammatories at immunosuppressive doses - immune mediated Surgical treatment - laser retinopexy (can prevent partial detachments from progressing e.g after cataract surgery) Similar approach might be performed to prevent progression in rhegmatogenous detachments. Retinal reattachment surgery may be offered at referral - pars plana vitrectomy with PFO silicone oil exchange and endolaser retinopexy. 70-90% retain vision post surgery in one study.

Answer 79

Fundus appears blurry in places Optic nerve head obscured by veil Blood vessels take abnormal turns Areas of hyperreflectivity

Answer 80

Retinal layers - round or dot haemorrhages Nerve fibre layer - flame shaped haemorrhages Subretinal layer - indistinctly bordered, diffuse dull red haemorrhages Superficial retinal vessels - keelboat haemorrhages, lead to vitreal separation Vitreal - dark shadowy areas obscuring view of retina, usually derives from adjacent tissue (uvea or retina), rare cases can be derived from persistent hyaloid artery/PHTVL/PHPV - these types of haemorrhages resorb slowly and increase risk of retinal detachment. Can provide valuable information for diagnosis and prognosis.

Answer 81

OCULAR: Trauma - scleral rupture, orbital fracture, blunt, intraocular surgery e.g phacoemulsification Congenital - CEA, persistent hyperplastic primary vitreous/hyaloid artery Uveal neoplasia SYSTEMIC: Cardiovascular - systemic hypertension, thrombocytopaenia, polycythaemia, coagulopathies, anaemic retinopathy, hyperviscosity syndrome Metabolic disease - diabetes mellitus Neoplasia - lymphoma, multiple myeloma, intracranial neoplasia, metastasis (mammary gland/thyroid/renal adenocarcinomas, malignant melanoma, haemangiosarcoma, rhabdomyosarcoma, neurogenic sarcoma, phaeochromocytomas) Other - granulomatous meningoencephalitis, meningoencephalitis of unknown origin, systemic lupus erythematosus

Answer 82

Blood pressure parameters <140 mmHg = normal 140-160 = pre-hypertensive 160-180 = hypertensive >180 = severe hypertension Common retinopathy of older cats (rare in dogs) Association with CKD and hyperthyroidism Ocular manifestations: Retinal vessel tortuousity Retinal oedema Retinal detachment Glaucoma Retina has small calibre vessels which make it susceptible to damage from prolonged systemic hypertension Treatment = control underlying hypertension and cause Amlodipine - calcium channel blocker = drug of choice for cats Repeat BP monitoring - once normotensive review BP at least every 6 months Hypertension control recommended even if not able to restore vision to prevent target organ damage. Vision recovery dependent on degree of damage and how quickly detected and treated - 70% of eyes with signs of retinal detachment reattached after hypertension treatment, little more than half the eyes without a menace response regained it. Prevention - annual fundic examination and blood pressure measurements in cats >10yrs recommended and more frequent checks for those with renal or thyroid disease.

Answer 83

Taurine deficiencies = cats Vitamin E deficiency = dogs (cocker spaniels)

Answer 84

Limited ability to synthesise taurine - need to get from diet Cats often present for dilated cardiomyopathy rather than ocular changes. Cats with cardiomyopathies - check fundus + taurine levels. 5 progressive stages of taurine deficiency visible on retina: 1. Increased granularity of area centralis 2. Ellipsoidal hyperreflective lesion in area centralis 3. Second hyperreflective lesion nasal to optic papilla 4. Both lesions merge into band of hyperreflectivity 5. Generalised retinal degeneration with attenuation of retinal vessels Occurs mainly in area centralis due to high density of photoreceptors in this area and high metabolic demand for taurine in this area. Histopathologically occurs in outer layers of retina Dietary correction can partially reverse the ERG changes but the lesions on the retina are permanent.

Answer 85

Various pathological changes in the muscle, CNS. reproductive tract and retina. Ophthalmoscopic signs = mottled tapetal fundus with discrete yellow-brown foci, hyperreflectivity and attentuation of retinal vessels. ERG may be non recordable at advanced stages but partially reversible with vitamin E supplementaton Histopathologically = accumulation of autofluorescent pigment in the RPE cells and photoreceptor damage over affected regions Connection between vitamin E deficiency and RPED in English Cocker Spaniels Bloods to detect alpha-tochophenol levels Supplementation can reverse neurological signs of ataxia and paresis but can only halt and not reverse retinal changes.

Answer 86

Ivermectin - especially collies/australian shepherds Enrofloxacin - cats

Answer 87

Collies/Australian Shepherds with mutation in multidrug resistance (MDR1) gene susceptible Clinical signs = acute blindness, dilated non-responsive pupils, retinal abnormalities - oedema, folds, low lying separation In some cases fundoscopy normal but retinal dysfunction can be confirmed on ERG Additional CNS signs may also be present. Exposure - history or plasma testing Intravenous lipid therapy - shown some effectiveness with some animals regaining vision within few hours Retinal scarring = common complication High doses >400mcg/kg = poor Can lead to death Lower doses some can have complete recovery

Answer 88

Cats treated with parenteral or oral enrofloxacin = can lead to acute retinal degeneration (Similar effects can be seen with orbifloxacin but not marbofloxacin) Affected patients - sudden acute blindness, dilated non responsive pupils, fundoscopic signs of hyperreflectivity and vessel attentuation. Absent ERG responses Susceptible cats have mutation in ABCG2 protein - component of blood-retinal barrier Genetic variation leads to accumulation of fluoroquinolone in the retina - generation of reactive oxygen species on exposure to light leading to retinal degeneration and blindness.

Answer 89

SARDS = sudden acquired retinal degeneration syndrome ONLY SEEN IN DOGS Leading cause of irreversible vision loss in dogs according to one study. Predisposed - obese, middle aged dogs of small breeds (<22kg) Spayed females over-represented Typical presentation - acute onset blindness, occuring over several days to weeks. Often other more systemic signs over longer period of time = lethargy + inattentiveness (mild visual changes before vision loss?) Weight gain, polyphagia, PUPD, skin and haircoat changes. hearing deterioration and decline in sense of smell (hence syndrome as affects multiple areas of body) Fundus appears normal.

Answer 90

Can be challenging as both conditions can present with acute blindness and a normal looking fundus. ERG = essential to differentiate Normal retinal responses with central blindness Extinguished flat line ERG with SARDS (loss of photoreceptor outer segments and apotosis of nuclei in outer nuclear layer affecting both rods and cones)

Answer 91

Unresponsive to red light but responsive to blue light stimulation. PLR's may respond slowly to bright light

Answer 92

Underlying cause = unknown, proposed ideas = endocrinopathy given systemic signs, toxicity, autoimmune inflammation (triggered by anti-retinal antibodies) No treatment for SARDS - dogs irreversibly blind but often good quality of life still. Polyphagia often to be main long term sign reported by O's Over time systemic signs tend to decrease leaving just blindness and polyphagia as the main remaining clinical signs.

Answer 93

Sudden severe visual deficits or blindness Extinguished retinal signal on ERG Relatively normal fundic appearance Develops as a paraneoplastic syndrome in which the cancer produces antibodies that mistakenly target the retina Loss of vision can occur before tumour diagnosis No evidence of cancer should be found in dogs with SARDS (2 conditions can appear similar) Should not all clinical features and diagnostic results fit with SARDs then this should be ruled out as differential diagnosis. Immunosuppression = good results for restoring vision in some cases.

Answer 94

Glaucoma = neurodegenerative disease Clinically see scotoma (blind spot) with intially peripheral vision loss followed by central vision loss. Acute cases retina can appear normal or show areas of oedema Severe retina damage can lead to retinal degeneration with pronounced thinning of the retina radiating from the optic nerve head. Cupping and atrophy of the ONH are common features (vasculature dips down into the ONH) Histopathologically glaucoma affects all retinal layers and progression occurs rapidly. Bowing of the lamina cribosa - compression of retinal ganglion cell axons, loss of axonal transport and death of RGC. Within day of glacoma onset = cells undergo necrosis followed by apoptosis and release of glutamate from dying cells - leads to further bystander injury. Spares tapetum but reason for this is not understood. ERG findins = greater decay of b wave amplitude during flash stimulation, a wave unaffected/

Answer 95

Primarily to address retinal detachments - aim to restore some vision or prevent complete blindness. Usually detachments secondary to - cataract surgery, lens luxations, cataracts and lens induced uveitis, retinal dysplasia, collie eye anomaly and trauma. Additional use - retrieving lens fragments that have dropped during cataract surgery.

Answer 96

Re-attachment of retina Prophylactic retinopexy - treatment of a normal fellow eye in cases of spontaneous retinal detachment, double row of non-contiguous burns on peripheral retina 360 degrees. Demarcation retinopexy - slow progression of nasal or temporal rhegmatogenous retinal detachment prior to referral for pars plana vitrectomy Barrier retinopexy - treating small tears or thin areas - indicated for horizontal or inferior retinal detachments but not superior detachments, less expensive than par plana vitrectomy but success rate is not as high - ideally should be referred for PPV if possible.

Answer 97

Retinopexy - cryotherapy or 810nm laser Best delivered in transpupillary fashion using the indirect ophthalmoscope Risks and complications - vitreous contraction, retinal holes, giant retinal tear

Answer 98

PPV used in giant retinal tears or giant dialyses (circumferential breaks of 90 degrees of more), typically detaching at the ora. - RHEGMATOGENOUS DETACHMENTS Giant tears PPV required as too advanced for demarcation retinopexy. <4 weeks reasonable chance of regaining some vision - sooner the repair the better the odds of vision Assessment before PPV surgery: Retinal health/conformation assessment, number of holes/tears PLR (positive = good prognostic indicator but can be misleading as some retinas detached for months can exhibit a response) ERG - not reliable at identifying surgical candidates, cases with extinguished ERGS may still be suitable candidates Recordable ERG however = good prognostic indicator Inflamed eyes - not good candidate due to high risk of failure/complications Aphakic eyes - issue with maintaining silicone oil in vitreous cavity Corneal scars/synechiae/capsular opacities impair vision EXUDATIVE TYPES OF RETINAL DETACHMENT NOT SUITABLE

Answer 99

1. Complete removal of the vitreous 2. Injection of either perfluorocarbon liquid or silicone oil to reposition the detached retina 3. Retinopexy laser to seal the retina around its periphery and randomly across its surface 4. If perfluorocarbon liquid used for better support it must be replaced silicone oil 70-90% success rate

Answer 100

Immune mediated/idiopathic - meningoencephalitis of unknown origin, isolated optic neuritis (white fluffy dogs), reactive histiocytic disease Infectious: Bacterial = direct extension e.g orbital abscess or bacteremia Protazoal = toxoplasma, neospora, ehrilichia, leishmania, rickettsia Parasitic - toxocara, angiostronglyus Neoplastic Primary - orbital meningioma, optic nerve glioma Secondary- direct invasion, orbital or CNS neoplasia, metastatic lymphoma Toxic - ivermectin, lead Traumatic - proptosis, blunt force, penetrating trauma Care (iatrogenic damage when draining retrobulbar abscess) Vascular & ischaemic - hypertension & glaucoma

Answer 101

Bilateral = sudden onset blindness (If normal looking fundus and sudden onset blindness - think SARDS or retrobulbar neuritis, slow more gradual onset of vision loss more typical of neoplastic compression or infiltration of pre-optic chiasm optic nerve) Main causes = immune mediated, idiopathic or infiltrative type disease (umbrella term meningoencephalitis of unknown origin MUO)

Answer 102

Swelling and oedema of the optic nerve head - blurring of its margins, peripapillary retinal oedema and vascular congestion/haemorrhages that are flame shaped as track along nerve fibres. May be accompanied by additional signs of ocular, orbital, CNS or systemic disease depending on aetiology. Chronic = pallor of optic nerve head, darkening or loss of neural tissue associated with end stage optic nerve degeneration.

Answer 103

Physical, ophthalmic and neurological examination (neuro exam important due to high frequency of MUO) ERG & Chromatic pupillary light reflexes - help differentiate from SARDS and retrobulbar optic nerve disease (ERG = normal with optic neuritis as photoreceptors intact) Rule out infectious disease - Haematology/Biochem/Serology MRI followed by CSF analysis

Answer 104

Infectious - specific antimicrobial therapy Immune mediated/idiopathic/infiltrative - immunosuppressive corticosteroids or other immunosuppressive drugs e.g cytoarabine Supportive treatments - anticonvulsants and fluid therapy to reduce increased intracranial pressure

Answer 105

Long term prognosis poor with only 30% of dogs regaining vision or retaining vision Prognosis worsens with delayed treatment and recurrent episodes - irreversible optic nerve damage.

Answer 106

1. Liquefaction - changes in the collagen and hyaluronic acid matrix - vitreous can separate more readily from retina potentially leading to retinal tears and rhegmatogenous retinal detachment. Can also enter anterior chamber increasing the risk of glaucoma 2. Proliferative vitreoretinopathy - response to retinal disease epiretinal cellular membranes may form which can contract and lead to traction retinal detachments 3. Vascularisation and cicatrisation - blood vessels may grow into the vitreous from an inflamed or malformed retina leading to vitreal haemorrhage 4. Elongation - visual deprivation during the neonatal period or due to cataracts and corneal opacities can lead to elongation of the vitreous body and axial length of the eye - this causes near sightedness (myopia)

Answer 107

Both conditions = small refractile bodies scattered throughout the vitreous Usually do not significantly impact vision Can occur spontaneously in older animals or secondary to chronic inflammatory or degenerative intraocular conditions. Asteroid hyalosis = calcium and phospholipid complexes - fixed in vitreous and move minimally with head or globe movements Synchysis scintillans = cholesterol, mobile within liquefied vitreous and can be seen as swirling snowflakes with head movements.

Answer 108

Originate from retinal or uveal blood vessels - Hypertensive retinopathy - Ocular trauma - Chorioretinitis - Intraocular neoplasia - Coagulopathies - Collie Eye Anomaly Small amounts resorb but larger amounts can persist for months and cause visual disturbances due to light scatter and interference. Treat underlying cause rather than haemorrhage itself?

Answer 109

Inflammation of the vitreous - often secondary to inflammation of nearby tissues Vitreous haze with cellular exudation, vitreous haemorrhage, liquefaction, epiretinal traction bands. Resolution of haze = indicator of effectiveness of treatment Address underlying cause of inflammation Drug delivery to vitreous tricky even systemically. Medical therapy ineffective - hyalocentesis (sample from vitreous) can be collected by specialist and submitted for culture, cytology, serology etc Severe case may recieve intravitreal injection or vitrectomy Infections can progress rapidly and lead to endophthalmitis, abscess or panophthalmitis Prognosis for vitreal infection = guarded

Answer 110

Rare disorder in cats AH misdirected into vitreous due to minute breaks in the hyaloid membrane acting as one way valves. Vitreous expands displacing lens, dilating pupil and leading to very shallow anterior chamber Tx = suppression of AH production with carbonic anhydrase inhibitors or in severe cases removing the lens and anterior vitreous.

Answer 111

COGS = neovascular membranes extending from optic nerve head and/or peripheral retina into vitreous along with clusters of glial cells lacking vascular supply. Exact cause not known but may be type of vitreoretinal dysplasia Hyphaema with secondary glaucoma = typical presentation Progresses to fulminant glaucoma with poor prognosis Labradors over-represented.