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Duke Elder > Retina and Vitreous > Flashcards

Retina and Vitreous Flashcards

1
Q

Revise diagram

A
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2
Q

Retina

A

The retina can be thought of as a direct extension of the brain. It is the out-sprouting of the optic nerve that reacts to light stimuli.

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3
Q

List the 3 main types of retinal neurons

A
  • Photoreceptors
  • Bipolar cells
  • Ganglion cells
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4
Q

Dimensions of the retina

A
  • Thinner temporally
  • Surface area of 1250mm2
  • Internally bound by vitreous
  • Externally bound by Bruch’s membrane of the choroid
  • Anteriorly continues with the outer pigmented choroidal epithelium (at the ora serrata)
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5
Q

Blood supply to the retina

A
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6
Q

Blood retinal barrier

A
  • Inner blood retinal barrier : tight endothelial junctions of retinal vessels
  • Outer blood retinal barrier: zonnulea occulodentes (Latin for tight junctions) of RPE
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7
Q

Retinal surface

A

Macula

  • 1.5mm
  • It has greater >1 ganglion cell layers compared to the peripheral retina which only has 1

Foveal avascular zone

  • 0.5mm
  • Avascular and depends on supply from the choriocapillaris via diffusion

Foveola

  • Fovea centralis (foveola) : 0.35mm
  • No rods but the maximum concentration of cones
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8
Q

What is the blind spot?

A

The blind spot is at the optic disc (contains no photoreceptors) and is 1.8mm2

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9
Q

2 principal components of the retinal structure

A
  1. The inner neurosensory retina
  2. The outer retinal pigment epithelium (RPE).
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10
Q

Revise image of OCT

A
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11
Q

Layers of the Neurosensory retina

A
  1. Internal limiting membrane
  2. Nerve fiber (contains ganglion cell axons)
  3. Ganglion cell layer (contains cell bodies of ganglion cells)
  4. Inner plexiform
  5. Inner nuclear (contains cell bodies of glial cells and bipolar cells)
  6. Outer plexiform
  7. Outer nuclear (contains cell bodies of photoreceptors)
  8. External limiting membrane
  9. Photoreceptors
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12
Q

RPE

A
  • The retinal pigment epithelium (RPE) lies outer to the photoreceptors
  • A single layer of cuboidal epithelium which maintains the photoreceptors
  • Bruch’s membrane of the choroid lies outer to the retinal pigment epithelium
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13
Q

How many layers total does the retina have?

A
  • The neurosensory retina has 9 layers.
  • The RPE is 1 layer.

In total, the retina is considered to have 10 layers.

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14
Q

2 main types of photoreceptors

A

Rods and cones.

Cones also come in 3 further subtypes

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15
Q

Compare rods vs cones

A

Ratio of rods: cones is 20:1

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16
Q

Retinal neuromodulator cells

A
  • These cells modulate action potentials
  • Horizontal cells : between photoreceptor and bipolar cells
  • Amacrine cells : between bipolar and ganglion cells
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17
Q

Ratio of photoreceptors to RPE cells

A

Ratio of photoreceptors to RPE cells is 45:1

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18
Q

Vitreous

A

The vitreous is a viscoelastic gel that fills the vitreous chamber - a 4ml cavity that forms the body of the eye. It is adherent to the retina and the ora serrata.

  • This gel is composed mainly of water, but also contains hyaluronic acid and type II collagen
  • It is connected to the internal limiting membrane of the retina by the collagen fibrils
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19
Q

What effect does age have on the vitreous

A
  • The vitreous gel progressively becomes runnier with age.
  • This is called syneresis and leads to small pools of fluid within the gel.
  • Syneresis can lead to posterior vitreous detachment from the retina.
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20
Q

Diabetic Retinopathy

A

Diabetic retinopathy is the most common microvascular complication of diabetes mellitus. The cause of visual impairment in patients with diabetic retinopathy is often due to diabetic macular oedema.

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21
Q

Pathology of Diabetic Retinopathy

A

The fundamental pathomechanism is: Hyperglycemia → damage to endothelial wall and pericytes
This process has several important effects:

  • Pericyte damage → microaneurysms → flame haemorrhages (nerve fibre layer)
  • Infarcts → cotton wool spots (axonal debris at infarct margins) (nerve fibre layer)
  • Increased vessel permeability → Hard exudates (lipoproteins in outer plexiform layer)
  • Cystoid macular oedema (outer plexiform layer)
  • Neovascularization
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22
Q

Most important risk factor for progression of diabetic retinopathy

A

The most important risk factor for the progression of diabetic retinopathy is the duration of diabetes

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23
Q

Presentation of DR

A

Most cases are picked up with diabetic screening but there are 3 associated presentations to be aware of:

  • Acute painful vision loss: Neovascular Glaucoma
  • Flashes/Floaters then painless vision loss: Vitreous haemorrhage or retinal detachment
  • Gradual vision loss: Retinopathy or macular oedema or cataract
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24
Q

Classification of Diabetic Retinopathy

A
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25
Q
A

Background retinopathy. Note the microaneurysms.

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26
Q
A

Proliferative retinopathy. Note the proliferation of the vasculature and the multiple haemorrhages.

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27
Q

Management of Diabetic Retinopathy

A

The management options are chosen based on risk classification

  • Non-proliferative → Monitoring
  • Proliferative → Panretinal photocoagulation (PRP) of the retina
  • Clinically significant maculopathy (including oedema) → Macular grid laser
  • Diabetic macular oedema → Anti-VEGF or OZURDEX® (steroid implant)

If the patient also has cataracts, treat diabetic complications before cataracts are addressed

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28
Q

Hypertensive Retinopathy

A

Chronic hypertension causes endothelial damage → atherosclerosis → constriction of retinal vessels → retinopathy.

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29
Q

Stages of hypertensive retinopathy

A
  1. Arteriolar narrowing
  2. AV nipping OR silver wiring
  3. Flame haemorrhages OR cotton wool spots
  4. Disc swelling OR hard exudates OR retinal oedema
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30
Q
A

AV nipping and arteriolar narrowing can be seen in this fundus photograph of a patient with hypertension.

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31
Q

Management of Hypertensive Retinopathy

A
  • Treatment is focused on targeting systemic hypertension.
  • Patients with papilloedema and malignant hypertension need emergency assessment
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32
Q

Compare CRAO vs BRAO

A
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33
Q

Compare CRVO vs BRVO

A
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34
Q

Retinal Artery occlusion

A
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35
Q
A

A fundus photograph of a patient with CRAO. Note the pale retina and the cherry-red spot.

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36
Q

Retinal Vein Occlusion

A

A fundus photograph of a patient with branch retinal vein occlusion.

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37
Q

Retinal Vein Occulusion

A
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38
Q

Ocular Ischemic Syndrome

A

Angina of the eye caused by severe carotid obstruction

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39
Q

Pathology of Ocular Ischemic Syndrome

A
  • Most commonly caused by atherosclerosis.
  • As with other causes of ocular ischemia, this can lead to neovascularization of intraocular structures such as the retina and iris.
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40
Q

Presentation of Ocular Ischemic Syndrome

A
  • The patient is typically an elderly male with a history of vascular risk factors such as diabetes, smoking and hypertension
  • Painful gradual reduction in vision with episodes of transient vision loss (amaurosis fugax) and orbital aching pain
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41
Q

Investigations for Ocular Ischemic Syndrome

A

Examination might show flare in the anterior chamber

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42
Q

Treatment of Ocular Ischemic Syndrome

A

Focused on relieving the carotid obstruction by stenting or endarterectomy

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43
Q

Sickle Cell Retinopathy

A

More prevalent in patients of Afro-Caribbean origin. Different mutations of Hb determine the severity of disease. HbSS is associated with the worst systemic disease and HbSC is associated with the worst ocular disease

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44
Q

Pathology of Sickle Cell Retinopathy

A
  • Sickling of cells leads to occlusion and ischemia. This can subsequently lead to proliferative changes and neovascularization.
  • Severity of disease is determined by mutation, from mild to severe: HbSC → HbSTHal → HbSS
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45
Q

2 Types of Sickle Cell Retinopathy

Compare presentation of each

A

Nonproliferative: Salmon patches (intraretinal haemorrhages and black sunbursts (RPE hyperplasia)

Proliferative: sea fan neovascularization, vitreous haemorrhage and retinal detachment

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46
Q

Classification system for proliferative sickle cell retinopathy

A

Goldberg classification

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47
Q

Management of Sickle Cell Retinopathy

A

Scatter laser photocoagulation can be used in severe sickle cell retinopathy

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48
Q

Compare Eales vs Coats Disease

A

These are 2 distinct retinal vascular diseases of unknown aetiology. They are frequently compared in exams.

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49
Q

What part of the visual field is the macula responsible for?

A

Central part of the visual field

Diseases of the macula characteristically present with reduced central vision

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50
Q

What is the commonest cause of blindness in the elderly (in developed countries)

A

Age Related Macular Degeneration (AMD)

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51
Q

What is AMD

A

The disease is limited to the macula and characterised by the presence of drusen.

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52
Q

Risk factors for AMD

A

Caucasian, female, elderly, smoking/hypertension

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53
Q

List 2 important genetic associations with AMD

A

CFH and ARMS2

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54
Q

Pathology of Dry AMD

A
  • Atrophy of RPE → accumulation of drusen between the RPE and Bruch’s membrane of the choroid.
  • Progression leads to geographic atrophy, which are large areas of visible choroid under the RPE.
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55
Q

Pathology of Wet AMD

A
  • Growth of choroidal vessels into the RPE (choroidal neovascularization).
  • Progression leads to disciform macular degeneration (subretinal fibrosis).
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56
Q

Pathology of Polypoidal choroidal vasculopathy (PCV)

A
  • A variant of Wet AMD
  • It is commoner in Asians
  • Unilateral polypoidal dilation of choroidal vessels progressing to subretinal haemorrhages
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57
Q

Most common cause of choroidal neovascularization

A

Wet AMD is the commonest cause of choroidal neovascularization. It is driven by retinal hypoxia.

In the case of wet AMD, it is caused by the build of drusen.

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58
Q

Presentation of wet vs dry AMD

A

Dry: Gradual central scotoma + gradually decreased visual acuity + drusen + metamorphopsia

Wet: Sudden central scotoma + neovascularization

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59
Q
A

Fundus photograph of a patient with AMD. Note the widespread drusen.

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60
Q

Investigations for AMD

A
  • OCT is used to detect drusen and areas of atrophy.
  • Geographic atrophy is best seen on fundus autofluorescence (FAF).
  • Amsler grid can be used by patients to self monitor their vision
  • Fundus fluorescein angiography (FFA) is used to assess wet AMD. OCT is also central to the diagnosis and monitoring of wet AMD.
  • FFA will show neovascularization and OCT will show subretinal fluid.
  • Indocyanine green angiography (ICG) is used to diagnose PCV, based on characteristic polypoidal dilation of choroidal vessels.
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61
Q

How is PCV specifically diagnosed

A

ICG is used to diagnose PCV because it is much better at imaging choroidal vessels compared to FFA because ICG is more closely bound to albumin and does not leak as much whilst passing through the choroidal vessels.

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62
Q

Management of AMD

A
  • Dry → AREDS2 diet (Vit C and E + Lutein + Zeaxanthin + Zinc)
  • Wet → Anti-VEGF intravitreal injections
  • Photodynamic therapy also plays a role in the management of wet AMD
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63
Q

What is Cystoid Macular Oedema (CMO)

A

This intraretinal oedema is s result of ocular inflammation, commonly in the post-cataract surgery phase.

It can also occur in other vascular and inflammatory disorders of the eye including diabetic retinopathy, uveitis, retinitis pigmentosa and latanoprost use.

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64
Q

Pathology of CMO

A
  • The mechanism of oedema is similar to elsewhere in the body, involving vessel hyper-permeability and high flow.
  • The fluid gathers within the intercellular spaces of the retina, most commonly the outer plexiform layer.
  • Macular oedema results in dVA because the fluid obstructs light.
65
Q

Presentation of CMO

A

Blurry vision + metamorphopsia + scotoma

66
Q

Investigation for CMO

A
  • Diagnosis is typically made by visualisation with OCT.
  • FFA can also be used and shows vessel leakage
67
Q
A

Cystoid macular oedema on OCT.

68
Q

Management of CMO

A

Treatment is stepwise and based on inciting injury. The mainstay is steroids.

  • Firstline: NSAIDS/steroid drops
  • If persisting after a month: continue topical + periorbital steroid injection (subtenon or orbital floor)
  • If persisting after another month: consider intravitreal or systemic steroids
  • Carbonic anhydrase inhibitors and anti-VEGF agents are used
69
Q

What is Central Serous Chorioretinopathy

A

Central serous chorioretinopathy is an idiopathic subretinal accumulation of fluid.

70
Q

Pathology of central serous chorioretinopathy

A

The exact mechanism is unknown but choroidal hyperpermeability is thought to play a role. This disease typically affects adult men under stress. It is also associated with steroid exposure.

71
Q

Pathology of central serous chorioretinopathy

A

The exact mechanism is unknown but choroidal hyperpermeability is thought to play a role. This disease typically affects adult men under stress. It is also associated with steroid exposure.

72
Q

Presentation of Central Serous Chorioretinopathy

A

Typically a middle-aged man with a stressful occupation who presents with a sudden unilateral reduction in visual acuity and scotoma.

73
Q

Investigation for Central Serous Chorioretinopathy

A

Diagnosis can be made by OCT which will show subretinal fluid collection with neurosensory retinal detachment.

74
Q
A

An OCT demonstrating central serous chorioretinopathy.

75
Q

Classic vignette for Central Serous Chorioretinopathy

A

A middle-aged man with a stressful job is the classic vignette for this condition.

76
Q

Management of Central Serous Chorioretinopathy

A

There is a high rate of spontaneous resolution, so specific treatment is only indicated in persistent cases over months with noticeable detriment to the quality of life

  1. Firstline → Argon laser
  2. If argon laser is unsuccessful → half dose photodynamic therapy (Verteporfin) may be considered
77
Q

Angioid Streaks

A

These streaks are sections of the Bruch’s membrane of the choroid that are calcified and broken.

  • Bilateral symmetrical irregular atrophied streaks from the optic disc to the outer retina.
  • Occur around the disc and can be visualised on FFA.
78
Q

Commonest cause of visual loss in Angioid Streaks

A
  • Breaks in Bruch’s membrane can lead to choroidal neovascularization which is most often the cause of visual loss in these patients
79
Q

Most common association with Angioid Streaks

A

The most common association is pseudoxanthoma elasticum

Patients present with yellow papules and wrinkling of skin folds around the neck, armpits and groin: ‘plucked chicken appearance’

80
Q

Most common association with Angioid Streaks

A

The most common association is pseudoxanthoma elasticum

Patients present with yellow papules and wrinkling of skin folds around the neck, armpits and groin: ‘plucked chicken appearance’

81
Q

Systemic associations with Angioid Streaks

A

PEPSI:

  • Pseudoxanthoma Elasticum
  • Pagets
  • Sickle cell
  • Idiopathic
82
Q

Degenerative Myopia

A

The term ‘degenerative myopia’ describes progressively myopic patients (> -6D of myopia) whose axial eye length does not stabilize with age i.e a progressive myopia. This is associated with various degenerative changes.

83
Q

Pathology of Degenerative Myopia

A
  • A progressively lengthening eye is associated with myopia, decreased visual acuity, posterior staphyloma and breaks in Bruch’s membrane (‘lacquer cracks’) - resulting in choroidal neovascularization and retinal detachments
  • Classically associated with connective tissue disorders
  • High myopia is the commonest cause of choroidal neovascularization in the young, compared to AMD in the elderly
84
Q

Presentation and examination findings of Degenerative Myopia

A
  • Presentation is a young patient with high myopia and decreased visual acuity.
  • Examination can show an unstably progressing axial length and the features above.
85
Q

Management of Degenerative Myopia

A
  • Time spent outdoors is protective
  • Choroidal neovascularization → Anti-VEGF intravitreal injection
86
Q

Retinitis Pigmentosa (RP)

A

RP is the commonest inherited retinal disorder. It is characterised by generalised photoreceptor dysfunction (rods first, then cones) and progressive atrophy of the retina.

87
Q

Most common mutation causing RP

A

RP is most commonly caused by a rhodopsin gene mutation on chromosome 3

88
Q

Most common mutation causing RP

A

RP is most commonly caused by a rhodopsin gene mutation on chromosome 3

89
Q

Presentation of RP

A
  • Nyctalopia + tunnel vision + decreased visual acuity
  • Associated with posterior subcapsular cataract, CMO, open-angle glaucoma and keratoconus
90
Q

Investigations for RP

A
  • A triad of fundoscopic findings: waxy disc + bony spicules + arteriolar attenuation
  • Optic disc drusen may be seen
  • ERG is electronegative - this is a helpful diagnostic finding and can also be used to monitor disease progression.
  • EOG is also abnormal because of global photoreceptor RPE dysfunction
91
Q

Compare ERG findings in RP

A

Initially, scotopic ERG (ERG in the dark) is worse than photopic (in the light) because rods are affected first.

92
Q
A

A fundus photograph of a patient with retinitis pigmentosa.

93
Q

Management of RP

A

No specific treatment is available as of yet but novel genetic therapies have shown promise in early clinical trials

94
Q

RP Associated Conditions

A
95
Q

What inherritance pattern are RP associated conditions

A

The RP associated conditions are inherited in an autosomal recessive fashion.

96
Q

Leber Congenital Amaurosis

A

Leber congenital amaurosis is a genetic cause of visual impairment in children. It is characterised by generalised dysfunction of photoreceptors.

97
Q

Pathology of Leber Congenital Amaurosis

A
  • AR severe rod-cone dystrophy.
  • Associated with multiple systemic features such as learning difficulty and epilepsy
98
Q

Presentation of Leber Congenital Amaurosis

A
  • Blindness at birth + nystagmus + absent pupil reflexes
  • Early disease → normal fundus
  • Late disease → Salt and pepper retinopathy + bulls-eye maculopathy
99
Q

Investigations for Leber Congenital Amaurosis

A

ERG is non-recordable because the photoreceptors are not working

100
Q

Best Disease

A

Best vitelliform macular dystrophy is the second commonest inherited macular dystrophy. It is characterised by a classic ‘egg yolk’ appearance of the macula.

101
Q

Pathology of Best Disease

A

AD mutation of the bestrophin gene on Chr11q13 → channelopathy of the RPE → abnormal lipofuscin accumulation and photoreceptor atrophy

102
Q

Presentation of Best Disease

A

Bilateral egg yolk macula (yellow circular elevated fundus lesion)

103
Q

Investigations for Best Disease

A
  • Characterised by an egg yolk macula on fundoscopy
  • ERG → Normal
  • EOG → abnormal with reduced Arden ratio

This is the classific cause of normal ERG with abnormal EOG.

104
Q

Stargardt Disease

A

Stargardt’s disease is the commonest inherited macular dystrophy and typically presents in childhood.

105
Q

Pathology of Stargardt Disease

A

AR mutation of ABCA4 on Chr1 l→ diffuse accumulation of lipofuscin in the RPE

106
Q

Presentation of Stargardt Disease

A

Reading difficulties in teenagers

107
Q

Investigations for Stargardt Disease

A
  • The fundus can appear normal in the early stage.
  • As the disease progresses, fundoscopy will show a beaten bronze macula with diffuse yellow specks
  • FFA shows a classically dark choroid due to blockage of fluorescence by lipofuscin
108
Q

Albinism

A

Albinism is the deficiency of melanin pigment. It can affect the eye in isolation (ocular albinism) or it can be systemic (oculocutaneous albinism).

109
Q

Pathology of Albinism

A
  • Oculocutaneous albinism (AR) is more common than ocular albinism (XL)
  • Decreased visual acuity is typically due to foveal hypoplasia
110
Q

Purpose of pigmentation in ocular structures

How does this relate to Albinism

A

Pigmentation is useful in ocular structures because it allows the careful filtering of light.

In ocular albinism, the iris and RPE are hypopigmented. This can lead to photophobia because too much light is bouncing around inside the eye.

111
Q

Presentation of Albinism

A

Presentation: dVA (foveal hypoplasia) + nystagmus + strabismus + iris hypopigmentation

112
Q

How do retinal fibres differ in ocular albinism

A

Interestingly, patients with albinism have been found to have an increased decussation of temporal retinal fibres at the optic chiasm, on visual evoked potentials

113
Q
A

(A) is a fundus in a patient with albinism. (B) is a normal fundus.

114
Q

Management of albinism

A

From an ocular perspective, the main priority is to treat the ametropia.

115
Q

Peripheral Retinal Degenerations

A

The majority of people have some sort of degeneration at the peripheral retina. Some of these people go on to develop breaks within the retina, which can affect vision.

116
Q

List 2 important types of peripheral retinal degenerations

A
  1. Lattice degeneration
  2. Degenerative retinschisis
117
Q

Compare Lattice degeneration
vs Degenerative retinschisis

A
118
Q

Where do the cysts in degenerative retinoschisis typically form

A

Between the outer plexiform and inner nuclear layers of the retina

119
Q

Retinal Tears

A

Retinal tears are full-thickness breaks through the retina. Retinopexy is used as treatment in cases which are high risk for progression into retinal detachment (RD). Tears are commoner in myopic eyes, because the surface area of the retina is greater.

120
Q

Compare the 3 different types of retinal tears

A
121
Q

What is the commonest cause of traumatic retinal detachment in children

A

Traumatic retinal dialysis

122
Q

Retinal Detachment

A

Retinal detachment is the separation of the neurosensory retina (NSR) from the retinal pigment epithelium (RPE). It is a serious condition that can lead to blindness.

123
Q

Classification of Retinal Detachment

A
124
Q

How is the NSR is attached to the RPE

A

Primarily by hydrostatic forces.

125
Q

Presentation of Retinal Detachment

A

Curtain fall vision loss, RAPD, Shaffer sign and Weiss ring (a sign of PVD)

126
Q

Investigations for retinal detachment

A
  • A recent detachment will appear on fundoscopy as a dome with loss of RPE markings
  • A chronic detachment will show a characteristic demarcation line
  • B scan ultrasound can be used if the view is obstructed (cataracts or vitreous haemorrhage)
  • Indirect ophthalmoscopy with scleral depression is used to visualise the ora serrata
127
Q
A

These fundus illustrations depict a Weiss ring (top) and chronic retinal detachment (bottom).

128
Q

Management of retinal detachment

A

Rhegmatogenous

  • Varies by situation and surgeon
  • Vitrectomy is the most commonly used procedure
  • Scleral buckling can be used if there is no evidence of PVD
  • Pneumatic retinopexy is used in cases of small tears between 11-1 clock hours

Tractional

  • Vitrectomy with membrane peel

Exudative

  • Aim to treat the underlying cause
129
Q

Posterior Vitreous Detachment

A

Separation of the posterior vitreous cortex from the internal retinal membrane

130
Q

Pathology of PVD

A

Liquefaction of the vitreous gel occurs with age → liquid seeps outside of the gel-matrix of the body of the vitreous → liquid accumulates between the outer membrane of the vitreous (vitreous cortex) and the internal limiting membrane of the retina.

  • This process is known as syneresis and eventually leads to the detachment of the vitreous from the retina.
  • This process can also lead to tearing of the retina and associated vessels, leading to vitreous haemorrhage
131
Q

What is Shaffer sign

A

If a retinal tear has occurred, pigmented retinal particles described as ‘tobacco dust’ can be seen in the vitreous.

This is known as Shaffer sign.

132
Q

Presentation of PVD

A
  • Patients typically present in old age with flashing lights and floaters in their vision.
  • Visual acuity tends to be preserved.
  • Weiss ring can be seen
133
Q

Why is it vitally important to look for tears in PVD

A

Because this dramatically increases the risk of RD.

134
Q

How are associated retinal tears (with PVD) treated

A

Associated retinal tears are treated with retinopexy (either laser or cryo)

135
Q

Management of PVD

A
  • PVD in itself does not require management other than vigilance for RD and its associated symptoms.
  • If the symptoms worsen or a visual field defect develops, they should immediately be investigated for RD.
136
Q

Vitreous Hemorrhage

A

Bleeding into the vitreous cavity

137
Q

Pathology of Vitreous Hemorrhage

A

Bleeding is either caused by traumatic injury or leakage during neovascular processes such as retinal vessel occlusion and DR

138
Q

Diagnostics of Vitreous Hemorrhage

A
  • Vision is obstructed by blood, easily seen on fundoscopy.
  • Full fundus examination is needed to look for retinal damage.
  • B scan can be used to evaluate the retina if the haemorrhage is extensive
139
Q

Management of Vitreous Hemorrhage

A
  • Fundal view present → PRP
  • Obstructed fundal view → Intravitreal anti-VEGF
  • Persistent haemorrhage or associated RD → Pars plana vitrectomy
140
Q

Hereditary Vitreoretinal Degenerations

A

Rare disorders are to be suspected in young patients who present with retinal/vitreous degenerations.

141
Q

List 3 Hereditary Vitreoretinal Degenerations

A
  1. X-linked Retinoschisis
  2. Stickler Syndrome
  3. Wagner Syndrome
142
Q

X-linked Retinoschisis

A
  • A genetic disorder characterised by abnormally weak adhesions between layers of the retina. This leads to the splitting of the retinal layers.
  • Often affects the nerve fibre layer
  • Typical presentation involves a young hyperopic boy with reading difficulties
  • Examination will reveal bilateral maculopathy resembling CMO but no leakage on FFA
  • Scotopic ERG will reveal a loss of the B wave
143
Q

How can Retinal detachment be distinguished from retinoschisis

A
144
Q

Stickler Syndrome

A
  • An AD disorder of type 2 collagen synthesis resulting in multiple systemic abnormalities including: deafness, marfanoid features, micrognathia and cleft palate
  • Ocular manifestations include: cataracts, ectopia lentis, glaucoma, RRD and empty vitreous
  • Patients are treated prophylactically with a retinal laser
145
Q

Wagner Syndrome

A
  • Similar to stickler but no systemic associations
  • Risk of RDD is much lower
146
Q

List and describe 4 other Vitreoretinal Disorders

A
147
Q
A

Normal OCT on the left and macular hole on the right.

148
Q

Peadiatric Leukocoria

A

Paediatric leukocoria is a white pupil or absence of a red reflex during the examination. It can be caused by: congenital cataract, retinoblastoma, persistent fetal vasculature, retinopathy of prematurity, Coats disease, and toxocariasis.

149
Q

Retinoblastoma

A
150
Q

Persistent Fetal Vasculature

A
  • Also known as Persistent hyperplastic primary vitreous
  • It is the failure of embryonic hyaloid artery regression.
  • Presentation: 2wks old + premature + unilateral leukocoria + microphthalmia + Mittendorf’s dot
151
Q

What is Mittendorf’s dot

A
  • Mittendorf’s dot is an examination finding of a posterior lens capsule opacity.
  • Bergmeister’s papilla is similar, but if it arises from the optic disc.
  • Both of these findings are related to the hyaloid artery
152
Q

Retinopathy of Prematurity

A

A retinal disease caused by oxygen therapy in premature infants

153
Q

Pathology of ROP

A
  • In utero, retinal vascular growth is driven by a relatively hypoxic state.
  • When premature infants are given oxygen therapy, the retinal vessels become disorganised and scarred. This can lead to RD and loss of vision
  • Retinal vessels reach the nasal ora serrata at 32 weeks and temporal serrata at 40 weeks. This means that the temporal retina is first affected because it is much weaker.
154
Q

Zone Classification of ROP

A
  • Zone 1 → radius 2x distance from disc to fovea with the disc at the centre
  • Zone 2 → Edge of 1 to nasal ora serrata
  • Zone 3 → From 2 to remaining retina
155
Q

Staging of ROP

A
  • White line demarcating avascular areas
  • Elevated thicker line
  • Extra retinal fibrovascular proliferation or neovascularization of the vitreous
  • Partial RD
  • Total RD
156
Q

What is plus disease

A

Plus disease → signs of vessel dilation or tortuosity

157
Q

Presentation of ROP

A

Premature infant + <1500g + birth hypoxia

158
Q

Screening for ROP

A
  • Screening: high-risk infants with indirect ophthalmoscopy using a 28D lens.
  • All infants <32 weeks gestation or <1500g are high risk
  • If born <27 weeks gestation → screen at 30 weeks
  • If born 27-32 weeks OR > 32 weeks + <1500g → screen 4 weeks postnatal
  • Stage 3 OR plus disease → screen weekly
  • Otherwise → screen 2 weekly
159
Q

Management of ROP

A

Transpupillary diode laser within 48 hours

Duke Elder (12 decks)

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