The Fundus Flashcards

1
Q

What are the 3 main layers which make up the fundus?

A
  1. Sclera (fibrous tunic - part of the uvea)
  2. Choroid with choroidal vasculature and pigmentation and the tapetum lucidum
  3. Retina with retinal pigment epithelium and translucent neurosensory layer and retinal vasculature.
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2
Q

What is the role of the sclera in the fundus?

A

Outmost layer of the fundus = provides structural support and protection to the inner eye components.

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3
Q

What is the role of the choroid in the fundus?

A

Choroid lies beneath the sclera - highly vascularised and responsible for supplying oxygen and nutrients to outer layers of the retina.

Also acts as a cooling system dissipating heat produced by light absorption.

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4
Q

What is the role of the tapetum lucidum?

A

Tapetum lucidium = present within the choroid
Enhances night vision by reflecting light back through the retina that has already passed through the retina once.

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5
Q

What is the innermost layer of the fundus and how is it divided?

A

Innermost = retina
Split into retinal pigment epithelium and neurosensory cells (including photoreceptors) - capture and process visual information before sending it to the brain via the optic nerve.

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6
Q

Describe the embryology of the retina - where is it derived from? When does the RPE and Neurosensory Retina develop?

A

Retina derives from posterior portion of optic cup
Differentiates from 2 layers of neuroectoderm origin

Outer layer = retinal pigment epithelium (fully developed day 25 gestation)
Inner layer = neurosensory retina (fully developed day 33)

Sub retinal space between these 2 layers is a potential gap and represents the location of most types of retinal detachment.

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7
Q

Where do the sclera, choroid and tapetum originate from embryologically?
Which structures are fully differentiated at birth and which continue to develop after birth?

A

Arise from neural crest mesenchyme which forms 2 layers.

Outer layer = sclera
Inner layer = choroid and tapetum

Sclera and choroid fully differentiated at birth
Tapetum continues to develop until about 4 months post partum

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8
Q

What is required to differentiate normally in order for the sclera and choroid to develop normally? What can we see if this doesn’t happen?

A

Retinal Pigment Epithelium need to differentiate correctly in order for choroid and sclera to form correctly.

If does not occur than can see uveoscleral colobomas with primary RPE abnormalities.

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9
Q

What are the 3 types of vitreous and what are their different roles?

A

Primary vitreous = contains hyaloid vasculature to nourish the embryonic lens. Hyaloid system should regress during last stages of development and before birth - condenses into Cloquet’s canal (clear narrow central zone) with closure of the foetal fissure.

Secondary vitreous = main portion of adult vitreous, develops with closure of the foetal fissure. Main composition - water, collagen, hyaluronic acid produced by peripheral hyalocytes.

Tertiary vitreous = contributes to development of the lens zonules at lens equator.

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10
Q

Describe the development of the optic nerve embryologically.

A
  1. Early embryogenesis retinal ganglion cells extend their axons towards the optic stalk gradually forming the optic nerve which exits the eye via the optic disc.
  2. A glial sheath forms around the hyaloid artery and as it regresses glial cells migrate into optic nerve
  3. Optic nerve reaches the brain on day 32
  4. Myelination begins at the chiasm, progresses to the eye and reaches the optic disc after birth
  5. Postnatally the optic nerve continues to mature and refine its connections with the brains visual centres to optimise visual function.
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11
Q

When does full fundic development occur?

A

Full fundic development does not occur until 8-10 weeks of age post natally.
Hence when eyelids open for first time the ophthalmoscopic appearance shows a lilac-blue colour throghout indicating the presence of an immature fundus that has not yet differentiated into tapetal and non tapetal zones.

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12
Q

How does the choroid receive its blood supply?

A

Short posterior ciliary arteries that enter the globe in the vicinity of the optic nerve

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13
Q

What type of animals may have visible choroidal vasculature as a normal variation and why?

A

Subalbionotic animals with blue eyes (dilution of ocular pigmentation) - no tapetum and no pigment in the RPE

Choroid visible as intricate meshwork of vessels radiating outwards from optic nerve head.
If no choroidal pigmentation either can see against the white of the sclera.

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14
Q

Describe the shape and appearance of the tapetum. Why is it visible normally and what is its function?

A

Part of the choroid
Roughly semicircular in shape
Variations in colour
Visible due to absence of melanin within the retinal pigment epithelium
Main function = reflect light that has already passed through the retina, restimulating photoreceptors and enhancing dim light vision.

Herbivores = fibrous tapetum
Carnivores = cellular tapetum

(Humans and other diurnal animals lack tapetum resulting in fundus that varies from red to orange to grey depending on amount of choroidal pigmentation)

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15
Q

How is the retinal pigment epithelium visualised on fundoscopy?

A

Can be visualised in the non tapetal fundus and is usually brown to black depending on the concentration of melanin granules in the cells.

Is still present across the whole fundus as part of the retina but lacks pigment in the tapetal section of the fundus usually.

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16
Q

How can disease affect the apperance of the RPE on fundoscopy?

A

Disease - can alter degree of pigmentation within theRPE

Inflammation, infection, degenerative processes within retina can all affect degree of pigmentation.

Hyperpigmentation - can be see in the tapetal fundus e.g chorioretinal scar (often encircled by tapetal hyperreflectivity due to thinning of the neurosensory retina)

Depigmentation - e.g RPE atrophy with retinal degeneration - depigmented or pale areas within the non tapetal fundus giving a mottled appearance.

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17
Q

What is the function of the RPE?

A

Outermost layer (facing choroid)
RPE supports retinal function by recycling used photopigment, storing Vitamin A for photopigment synthesis, renewing outer segments of photoreceptors and acting as part of the blood-retina barrier for ocular immune defence.

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18
Q

Why can we not directly visualise the neurosensory retina on fundoscopy? How can we detect changes to this layer instead?

A

Cannot directly visualise as translucent.
Instead as it lies over the tapetum it reduced the reflectivity of the tapetum and makes the non tapetal areas slightly greyer than frank brown/black.

Thinning of the retina (often associated with retinal degeneration) = increased reflectivity of the tapetum (hyperreflectivity)

Thickening - (cellular infiltration/subretinal space fluid accumulation) leads to hyporeflectivity

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19
Q

What are the 10 layers that make up the retina from outermost (facing choroid) to innermost (facing vitreous).

A
  1. Retinal Pigment Epithelium (RPE)
  2. Photoreceptor layer - inner and outer segments of rods and cones and where vision initiation occurs. Photoreceptors absorb light photons through photopigment, triggers complex biochemical cascade that generates neuronal signal - process if called phototransduction.
  3. External limiting membrane - separates photorecptor layer from their nuclei
  4. Outer nuclear layer - contains nuceli of rods and cones
  5. Outer Plexiform layer - synaptic layer - axonal extensions of photoreceptors form synaptic expansions. Synapse with bipolar, horizontal and adjacent photoreceptors cells. Plays a role in early visual signal processing.
  6. Inner nuclear layer - contains nuclei of bipolar, horizontal and Mullers and amacrine cells.
    Bipolar cells = synapse with photoreceptors - relaying visual signal to internal retina and retinal ganglion cells
    Horizontal and amacrine cells - modulate neuronal activity in the outer and inner retina
    Muller cells - span entire retina providing structural support and other physiological functions.
  7. Inner plexiform layer - second synaptic layer - synapses between bipolar, amacrine and retinal ganglion cell dendrites enabling complex processing of the visual signal
  8. Ganglion cell layer = cell bodies of retinal ganglion cells (axons for the optic nevrve)
  9. Optic nerve fibre layer - retinal ganglion cell axons converging on the optic disc to form the optic nerve transmitting visual signals to the brain
  10. Internal limiting membrane - Innermost retinal layer adjacent to the vitreous, basement membrane to which the inner ends of Mullers cells are attached.
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20
Q

Why is the retina arranged in what seems a counterintuitive fashion with the RPE and photoreceptors being in outermost and the retinal ganglion cells the innermost?

A

This arrangement is most likely due to the high metabolic demands of the photoreceptors meaning they need close proximity to their blood supply the choroid.

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21
Q

What is the dual blood supply of the retina?

A

Photoreceptors supplied by the choroid
Inner retina supplied by the retinal vessels

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22
Q

Which types of animal have the following types of fundus?

Merangiotic
Pauangiotic
Holangiotic
Anangiotic

A

Merangiotic = rabbit (horizontal retinal vasculature)
Pauangiotic = horse (30-60 short retinal vessels surrounding the optic nerve)
Holangiotic = dogs and cats
Anangiotic = birds

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23
Q

Describe the retinal vasculature anatomy in the cat.

A

3 major pairs of cilioretinal arteries and veins
Originate around the periphery of the optic disc
Arcing around the area centralis they create a seemingly vessel free zone although a capillary network does still exist.

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24
Q

Describe the retinal vasculature anatomy in the dog.

A

20 cilioretinal arterioles radiating from the optic disc along with 3-4 major veins
Partial venous circle present on the optic disc (unlike cats)
Area centralis appears free of vasculature
Retinal vessels more tortuous than in other species.

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25
Q

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

A

Intraocular
Intraorbital
Intracanicular
Intracranial

Optic nerve consists of ganglion cells axons surrounded by myelin.

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26
Q

What type of flow is important for optic nerve function and at what pressure if this flow interrupted?

A

Axoplasmatic flow = important for optic nerve function and metabolism but pressure sensitive

> 50mmHG = no flow

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27
Q

What is the optic nerve head (also known as optic disc/optic papilla)? Where is it located on the fundus?

A

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.

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28
Q

What things can affect the visibility and appearance of the optic nerve head as normal variations?

A

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.

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29
Q

What is the physiologic cup or pit on the optic nerve head?

A

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)

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30
Q

What is the role of the vitreous and what is it composed of?

A

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.

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31
Q

Define the following:
Scotopic vision
Mesopic vision
Photopic vision

How can this relate to ERG?

A

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.

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32
Q

What determines the richness of colour vision?

A

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.

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33
Q

How does the colour vision of the following species vary?
Humans & Primates
Dogs & Cats
Horse
Reptiles & Avians

A

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)

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34
Q

What is visual acuity and how is it provided?

What is the area centralis/visual streak? What do birds have instead?

A

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.

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35
Q

Why does the tapetum lead to a reduction in visual acuity?

A

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

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36
Q

Which photorecptor type is primarily responsible for detection of motion?

A

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

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37
Q

What methods are there for assessment of the fundus and how should fundic assessment ideally be performed?

A

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,

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38
Q

Compare and contrast direct and indirect ophthalmoscopy methods of visualising the fundus.

A

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.

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39
Q

What is electroretinography (ERG)? What is it used for?

A

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)

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40
Q

What do the ERG responses vary based on? How do we utilise this to look at the rods/cones.

A

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

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41
Q

What equipment is required to perform an ECG?

A

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

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42
Q

What waveforms do we typically see with a normal ERG?

What does a flat line on an ERG indicate?

A

A wave = photoreceptor response

B wave = bipolar cells

C wave = retinal pigment epithelium

Flatline on an ERG = peripheral blindness

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43
Q

What factors may influence the ERG readings?

A

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.

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44
Q

What modality can we use to evaluate the fundus when ophthalmoscopy is not possible (e.g due to mature cataracts, hyphaema, severe corneal oedema etc)

A

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)

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45
Q

What modality would we want to use to examine the optic nerve itself?

A

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

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46
Q

What is the chromatic pupillary light reflex and what do we use it for?

A

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.

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47
Q

What two methods do we have for screening for inherited eye disease?

A

DNA testing
Eye examinations

The two should be used complementarily

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48
Q

Describe how eye examinations for inherited diseases are performed.

A

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.

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49
Q

How can DNA testing be used for screening for inherited eye disease. What are the 2 types of test and what are the advantages of using DNA tests.

A

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

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50
Q

Compare and contrast the use of DNA testing vs Eye Examination for screening for inherited eye disease.

A

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

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51
Q

Describe PHPV/PHTVL (persistent hyperplastic primary vitreous)

Which breeds are predisposed.

A

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.

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52
Q

What is retinal dysplasia?

A

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)

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53
Q

What mode of inheritance causes the majority of retinal dysplasias?

A

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

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54
Q

What are the 2 main appearances of retinal dysplasias? How do they affect vision

A

Multifocal retinal dysplasia vs Total retinal dysplasia

Multifocal = vision normal in many dogs

Total = blindness

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55
Q

Describe multifocal retinal dysplasia (MRD)

A

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.

56
Q

Describe the histopathology of MRD.

A

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.

57
Q

Describe geographic retinal dysplasia. What is it a subtype of?

A

Geographic retinal dysplasia = subtype of multifocal retinal dysplasia

Circular areas of dysplastic retina
Commonly observed dorsal to optic disc in tapetal fundus

58
Q

Is retinal dysplasia usually progressive and can the lesions change over time?

A

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.

59
Q

At what age would you generally screen for retinal dysplasia?

A

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.

60
Q

Which breeds are predisposed to multifocal retinal dysplasia?

A

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

61
Q

Describe total retinal dysplasia.

What other ocular abnormalities may it be associated with?

A

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

62
Q

Which breeds are predisposed to the total form of retinal dysplasia?

A

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.

63
Q

What other causes are there for retinal dysplasias apart from inherited forms?

A

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

64
Q

What is Collie Eye Anomaly (CEA) - how does it usually present

A

Congenital disorder (complex) affecting retinal, choroidal and scleral development

Bilateral disease but not usually symmetrical in presentation.

65
Q

What is the hallmark sign of Collie Eye Anomaly and where is this sign typically seen?

A

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.

66
Q

Why can Collie Eye Anomaly appear to ‘go normal’? When is eye testing for predisposed breeds recommended due to this.

A

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.

67
Q

Which breeds are predisposed to Collie Eye Anomaly?

A

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

68
Q

What other fundic abnormalities may be seen as part of the extended Collie Eye Anomaly phenotype?

How do they affect vision?

A

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.

69
Q

What is optic nerve aplasia and optic nerve hypoplasia?

A

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.

70
Q

What is an optic nerve coloboma and how do they appear? What breeds can it be seen in?

A

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.

71
Q

What is PRA and how is it characterised?

What are the 2 main types of PRA

A

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.

72
Q

What is the typical clinical presentation in cases of PRA?

What other ocular disease can be complications of PRA?

A

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.

73
Q

What is the most common form of PRA? What is its mode of inheritance.

A

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

74
Q

How is PRA usually diagnosed?

A

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.

75
Q

How are PRA’s normally classified?

What is the genetic and molecular pathogenesis for PRA?

A

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.

76
Q

Is there any treatment for PRA? How can we prevent PRA?

A

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.

77
Q

List some breeds commonly affected by PRA according to the BVA Eye Scheme.

A

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

78
Q

What is Achromatopsia/Hemeralopia? Which breeds are affected?

How does it appear on ophthalmic exam and how is it diagnosed?

A

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

79
Q

What is Retinal Pigment Epithelial Dystrophy (RPED)?
Does this disease cause blindness?
Which breeds are affected?
What vitamin deficiency can it be associated with - how can this be detected?

A

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)

80
Q

What is retinal dystrophy in Briards? How does it present?

What therapy is currently being studied for this disease?

A

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

81
Q

What is Canine Multifocal Retinopathy? (CMR)

Which breeds are affected?

A

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.

82
Q

List all the inherited types of retinal/fundic disease seen in dogs.

A

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

83
Q

List the inherited retinal diseases seen in cats.

A

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

84
Q

Describe early onset rod-cone dysplasia in cats (Rdy).

A

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.

85
Q

Describe late onset rod-cone degeneration in cats. Which breed does it mainly affect?

A

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.

86
Q

Why does inflammation of the choroid often affect the retina leading to chorioretinitis and vice versa?

How else is chorioretinitis often referred to?

A

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.

87
Q

What type of disease generally tends to cause chorioretinitis?

A

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

88
Q

What are the ophthalmoscopic findings associated with chorioretinitis?

A

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

89
Q

What are the ophthalmoscopic findings associated with inactive chronic chorioretinitis?

A
  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.
90
Q

How should you work up a case of suspected chorioretinitis?

A

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
91
Q

List the causes of chorioretinitis.

A

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

92
Q

How do we treat chorioretinitis?

A

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

93
Q

List the infectious cause of chorioretinitis in dogs.

A

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

94
Q

List the infectious causes of chorioretinitis in cats.

A

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

95
Q

Define retinal detachment.

A

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.

96
Q

What are the 3 main types of retinal detachment - describe the ophthalmoscopic findings with each type.

A
  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

97
Q

What is the classical sign of retinal detachment on ultrasound often termed?

A

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.

98
Q

How can the ERG of a patient with retinal detachment appear?

A

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

99
Q

List the common causes for retinal detachment.

A

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

100
Q

Why do patients with retinal detachments still sometimes have an intact (but sluggish) PLR?

A

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.

101
Q

How do we work up cases of retinal detachment?

A

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)

102
Q

How can we treat cases of retinal detachment?

A

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.

103
Q

What signs on fundoscopy should make you suspicious for a retinal detachment?

A

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

104
Q

How can retinal/vitreal haemorrhages be localised based on their appearance?
Why can localising retinal/vitreal haemorrhages be useful?

A

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.

105
Q

List the causes for retinal and vitreal haemorrhages

A

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

106
Q

Describe hypertensive retinopathy in the cat.

A

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.

107
Q

Which nutritional deficiencies can lead to retinopathies?

A

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

108
Q

Describe taurine deficiency retinopathy in the cat.

A

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.

109
Q

Describe Vitamin E deficiency retinopathy in the dog.

A

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.

110
Q

Which drugs can cause retinopathies in the dog and cat.

A

Ivermectin - especially collies/australian shepherds
Enrofloxacin - cats

111
Q

Describe ivermectin toxicity in the dog with respect to the retina. How would you treat?

A

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

112
Q

Describe enrofloxacin toxicity in cats.

A

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.

113
Q

Describe SARDS - why is it a syndrome?

A

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.

114
Q

How can you differentiate SARD’s from central causes of blindness?

A

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)

115
Q

How do dogs with SARDs respond to the chromatic pupillary light reflex tests?

A

Unresponsive to red light but responsive to blue light stimulation.

PLR’s may respond slowly to bright light

116
Q

What is the cause for SARDS? Is there any treatment for SARDS?

A

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.

117
Q

What is autoimmune retinopathy/cancer associated retinopathy? What is the main ddx for this disease. How can it be treated/managed.

A

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.

118
Q

Why does retinal degeneration occur with glaucoma?

A

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/

119
Q

What are the main indications for vitreoretinal surgery?

A

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.

120
Q

What is retinopexy and what are the different types of retinopexy?

A

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.

121
Q

How is retinopexy performed and what are the risks and complications?

A

Retinopexy - cryotherapy or 810nm laser
Best delivered in transpupillary fashion using the indirect ophthalmoscope

Risks and complications - vitreous contraction, retinal holes, giant retinal tear

122
Q

What is pars plana vitrectomy used for?
What is the prognosis for this surgery depending on time detached?
How are candidates assessed pre-surgery?

A

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

123
Q

Describe briefly how Pars Plana Vitrectomy is performed.

What is the success rate with visual outcome?

A
  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

124
Q

List the causes of optic neuritis in the dog.

A

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

125
Q

What are the usual presenting signs of optic neuritis? What are the main causes of optic neuritis?

A

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)

126
Q

How does the optic nerve head appear in cases of optic neuritis?

What other types of signs may accompany?

How does the optic nerve head appear with chronic optic neuritis?

A

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.

127
Q

How do we work up and diagnose the cause of optic neuritis?

A

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

128
Q

What treatments are there for optic neuritis?

A

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

129
Q

What is the prognosis for optic neuritis in terms of regaining vision?

A

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.

130
Q

What are the 4 pathological reactions the vitreous can exhibit?

A
  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)
131
Q

What are asteroid hyalosis and Synchysis scintillans? How can we tell apart?

A

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.

132
Q

What factors can cause vitreal haemorrhages?

How quickly does blood resorb from the vitreous.

A

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?

133
Q

What is hyalitis/vitritis and what are the underlying causes?

How may it be treated?

A

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

134
Q

What is aqueous misdirection syndrome (malignant glaucoma) and which species does it affect. How is it treated?

A

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.

135
Q

What is canine ocular gliovascular syndrome and how does it appear?

A

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.