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Clinical Opthalmology > Retina > Flashcards

Retina Flashcards

1
Q

Risk factors of diabetic retinopathy

A
  • duration of diabetes
  • poor control of diabetes
  • pregnancy
  • hypertension
  • nephropathy
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2
Q

DR Pathogenesis

A
  • microangiopathy in which small BV’s are vulnerable due to high glucose levels
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3
Q

Diabetic retinopathy classification

A
  • background DR (microaneurysms and blot haemorrhages)
  • diabetic maculopathy (retinopathy at macula- Oedema and ischemia)
  • preproliferative DR (cotton wool spots, venous changes, often deep haemorrhages)
  • proliferation diabetic retinopathy (neovasularisation within 1 or more disc diameters)
  • advanced diabetic eye disease (tractional retinal detachment, vitreous haemorrhage, neovasular glaucoma)
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4
Q

Scottish DR grading scheme

A
  • R0 (no DR)
  • R1 (background DR mild) - 12 month check
  • R2 (Background DR - observable) - 6 month check
  • R3 (Background DR referable) - refer
  • R4 (Proliferative DR) - refer
    ————————————————
  • M0 - no maculopathy
  • M1 - observable, any hard exudates
  • M2 - referable, any blot haemorrhages or exudates
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5
Q

Diabetic retinopathy signs

A
  • Microaneurysms
  • retinal haemorrhages
    >NFL, intra-retinal, deep haemorrhage
  • exudates
  • diabetic macular oedema
  • cotton wool spots
  • Venous changes (general dilation and tortuosity, looping, beading, sausage like segmentation)
  • intra-retinal microvascular abnormalities (IRMA)
  • artery dilation
  • Proliferative retinopathy
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6
Q

Diabetic Maculopathy, M1 and M2 presentation

A
  • M1 - Earliest stage of maculopathy, exudates visible but more than a disc diameter from fovea so unlikely to affect vision soon
  • M2 - Exudates are close to the fovea, VA reduced, OCT will show central foveal thickness exceeds 300 microns, needs to be treated
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7
Q

Treatment of DR

A
  • Px education
  • Diabetic control
  • Control other risk factors - hypertension
  • Quit smoking

Treatment of Macular oedema
- anti-VEGF injections (some px’s require continuous injections as oedema reoccurs when injections stop)
- laser photocoagulation
- sub threshold diode laser

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8
Q

Retinal Vein Occlusion Risk Factors

A
  • age
  • hypertension
  • hyperlipidaemia
  • diabetes
  • glaucoma
  • OCP
  • smoking
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9
Q

Branch Retinal Vein Occlusion Signs

A
  • If macular involvement - sudden onset painless blurry vision and metamorphopsia
  • iris neovascularisation

FUNDUS
- Dilation and tortuosity of affected segment
- blot haemorrhages
- cotton wool spots
- retinal neovascularisation (8% risk)
- chronic macular oedema
- pre-retinal and vitreous haemorrhages
- potential RD

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10
Q

Branch Retinal Vein Occlusion Management

A
  • treat hypertension if underlying cause (routine referral to GP for management of risk factors)
  • intra-retinal anti-VEGF agents
  • intravitreal defame those implant
  • laser to the macula
  • review
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11
Q

BRVO Prognosis

A
  • 50-60% of Px maintain a VA better than 6/15
  • Poorer prognosis if there is macular oedema or neovascularisation- 25% have VA of 6/60
  • BRVO in one eye increases the risk of it happening in the other eye
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12
Q

Non Ischemic CRVO signs/symptoms

A
  • sudden monocular decrease in vision
  • RAPD (mild or none)

FUNDUS
- signs present in all quadrants
- tortuosity and dilation
- Cotton wool spots
- dot/blot and flame haemorrhages
- optic disc and macular oedema
- patchy ischemic retinal whitening at posterior pole

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13
Q

Ischemic Central Retinal Vein Occlusion

A
  • Characterised by substantially decreased retinal perfusion with capillary closure and retinal hypoxia
  • more severe than non-ischemic with RAPD present and more severe visual loss
  • optociliary shunts
  • pain, photophobia due to neovascular glaucoma
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14
Q

Hemiretinal Vein occlusion

A
  • Involves the occlusion of the inferior or superior branch of the central retinal vein
  • prognosis depends on level of Ischemia
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15
Q

Hemiretinal vein occlusion signs

A
  • sudden altitudinal visual field defect
  • reduction in VA (depends on location)
  • neovascular iris
  • similar FUNDUS features to BRVO

FUNDUS (BRVO)
- Dilation and tortuosity of affected segment
- blot haemorrhages
- cotton wool spots
- retinal neovascularisation (8% risk)
- chronic macular oedema
- pre-retinal and vitreous haemorrhages
- potential RD

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16
Q

CRVO treatment

A

Treatment of macular oedema
- intraretinal anti VEGF agents
- Intravitreal dexamethasome implant

Treatment of neovascularisation
- panretinal photocoagulation (1500-2000 burns spaced a burns width apart, avoiding areas of haemorrhage)
- anti VEGF injections every 6 weeks
- regular check ups to observe if neovascular glaucoma develops

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17
Q

Amaurosis Fugax

A
  • painless monocular loss of vision
  • curtain ominous over the eye
  • can be caused by an embolus, it can be neurological, ocular, hemodynamic and idiopathic
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18
Q

Branch Retinal Artery Occlusion signs

A
  • profound painless altitudinal or sectorial visual field loss
  • may go unnoticed if central vision is spared
  • VA is variable, if central vision is affected then poor prognosis
  • RAPD
  • Attenuation (reduced output) of arteries
  • segmentation
  • cloudy white oedematous retina corresponding to the area of ischemia, potential blood column
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19
Q

Central Retinal Artery Occlusion Signs

A
  • sudden profound loss of vision
  • VA - severely reduced
  • Poor prognosis in all cases
  • profound RAPD sometimes amaurotic pupil
  • Attenuation (reduced output) of arteries
  • segmentation
  • cloudy white oedematous retina corresponding to the area of ischemia, potential blood column
  • Cherry red spot (in first 48 hrs)
  • Visible emboli (20% of cases)
  • 2% develop neovasculaisation
  • Rubeosis iridis
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20
Q

Cilioretinal Artery Occlusion

A
  • cilioretinal artery present in 1/3 of eyes, providing the central macula with a second arterial blood supply
  • its main importance is when it preserves the central vision after a CRVO
  • Isolated CRAO is rare
  • Combined with CRVO
  • Combined with AION - very poor prognosis
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21
Q

Treatment of Acute Retinal Artery Occlusion

A
  • Emergency as it can cause irreversible visual loss unless the retinal circulation can be re established
  • ocular massage with 3 mirror contact lens
  • anterior chamber paracentesis
  • Breathing high oxygen (95%) and (5%) carbon dioxide
  • Thrombolysis
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22
Q

Ocular Ischemic Syndrome

A
  • results from chronic ocular hypoperfusion (reduced blood flow), secondary to severe ipsilateral carotid stenosis
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23
Q

Ocular Ischemic Syndrome Signs

A
  • gradual loss of vision over weeks
  • ocular and periocular pain
  • 2% will deteriorate to light detection within 1 year
  • episcleral injection and corneal oedema
  • aqueous flare
  • iris atrophy and rubeosis iridis
  • venous dilation
  • arteriolar narrowing
  • Proliferative retinopathy
  • Macular oedema
  • neovascular oedema
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24
Q

Ocular Ischemic Syndrome management

A
  • anterior segment inflammation is treated with topical steroid and a mydriatic as appropriate
  • Proliferative retinopathy is treated with panretinal photocoagulation
  • Macular oedema is treated with anti-VEGF agents
  • carotid surgery - stent
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25
Q

Types of Hypertensive eye disease

A
  • Retinopathy
  • Choroidopathy
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26
Q

Hypertensive Eye Disease - Retinopathy grading system

A
  • arteries constrict under ocular hypertension
  • Grade 1 - mild generalised retinal arteriolar narrowing
  • Grade 2 - Focal anteriolar narrowing, AV nipping, copper wiring
  • Grade 3 - Grade 2 plus retinal haemorrhages, exudates and cotton wool spots
  • Grade 4 - Severe grade 3 plus OD swelling, which is a marker of malignant hypertension
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27
Q

Hypertensive retinopathy prognosis

A
  • Px at higher risk of coronary disease and peripheral vascular disease
  • mortality in malignant hyper tension is 50% over 2 months and 90% in 1 year
  • increased risk of RAO and RVO
  • damage to optic nerve and macula has long term reductions in VA
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28
Q

Hypertensive Retinopathy Management

A
  • Grade 1+2 - referral to GP for BP check
  • focus on reducing blood pressure
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29
Q

Hypertensive Eye Disease - Choroidopathy

A
  • Siegrist Streaks, flecks arranged linearly along choroid all vessels and are indicative of fibrin oil necrosis
  • Elsching spots are focal choroidal infarcts seen as small black spots surrounded by yellow haloes
  • Exudative retinal detachments, sometimes bilateral, may occur in acute severe hypertension such as that associated with toxaemia of pregnancy
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30
Q

Sickle cell Retinopathy

A
  • Caused by abnormal haemoglobins that induce RBC to adopt an anomalous shape under conditions of physiological stress such as hypoxia (low levels of oxygen)
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31
Q

Sickle cell Retinopathy - Non Proliferative Retinopathy

A
  • venous changes (tortuosity, RVO is uncommon)
  • arteriolar changes, occlusions can involve branch, central or macular vessels. Silver wiring and corkscrewing of peripheral vessels
  • optic disc, dark red blots on the disc surface due to small vessel occlusion
  • salmon patches, orange-red superficial haemorrhages
  • macular depression sign, oval depression in the temporal macular retina due to retinal thinning
  • peripheral areas of whitening
  • angioid streaks
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32
Q

Sickle cell Retinopathy - Proliferative Retinopathy

A

Usually presents no symptoms unless there is a vitreous haemorrhage or retinal detachment

  • stage 1, peripheral arteriolar
  • stage 2, peripheral arteriovenous anastomosis proximal to non-perfused areas
  • stage 3, sea fan neovascularisation develops at the edge of perfused retina, usually with a single draining venule. Disc neovascularisation may rarely occur.
  • stage 4, vitreous haemorrhage from the NV
  • stage 5, rhegmatogenous retinal detachment caused by a retinal break associated with extensive fibrovascular proliferation
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33
Q

Sickle Cell Retinopathy - Management

A
  • observation if vitreous haemorrhage has not occurred
  • laser or cryotherapy ablation of peripheral non-perfused retina
  • vitreoretinal surgery May be required for tractional retinal detachment
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34
Q

Retinopathy of Prematurity

A
  • Affects low weight infant
  • early exposure to high ambient oxygen concentration appears to be a key risk factor
  • Occurs as retinal vascularisation not complete till about 36 weeks
  • If baby born before that, peripheral retina will be ischaemic, leading to upregulation of VEGF and new BV formation
    - More peripheral than diabetic new BV’s
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35
Q

Stages of Retinopathy of Prematurity

A

Describes the abnormal vascular response at the junction of immature a vascular peripheral and vascularised posterior retina

Stage 1- a thin, flat, tortuous, grey white lines running roughly parallel with the ora serrata
Stage 2 - height and width extends above the plane of the retina
Stage 3 - extraretinal fibrovascular proliferation extends from the ridge into the vitreous
Stage 4 - partial retinal detachment is divided into foveal and extrafoveal
Stage 5 - total retinal detachment

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36
Q

Retinopathy of prematurity treatment

A
  • cryotherapy
  • anti VEGF agents
  • Pars plana vitrectomy
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37
Q

Primary Retinal Telangiectasia

A

Develops secondary to vascular compromise
Comprises a group oof rare, idiopathic, congenital or acquired retinal vascular anomalies characterised by dilation and tortuosity

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38
Q

Retinopathy in blood disorders

A
  • Leukaemia
  • Anaemia
  • Hyperviscosity
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39
Q

Retinopathy in blood disorders - Leukaemia and its major variants and signs

A

Malignancies of haematopoietic stem cells, involving abnormal proliferation of white blood cells

Major varients of leukaemia
- acute lymphocytic predominantly affects children
- Acute myeloid is seen in older adults
- Chronic lymphocytic, many Px die of unrelated disease
- chronic myelocytic has a progressive clinical course and less favourable prognosis

Ocular Features
- retinal haemorrhages and cotton wool spots
- Roth spots are retinal haemorrhages with white centres
- peripheral retinal neovascularisation
- optic nerve infiltration may cause swelling and visual loss
- subconjunctival haemorrhage and cranial nerve palsy’s

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40
Q

Retinopathy in blood disorders - anaemia

A

Decrease in the number of circulating red blood cells or amount of haemoglobin in each cell

Retinopathy
- venous tortuosity
- haemorrhages

Optic neuropathy
- may occur in pernicious anaemia

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41
Q

Retinopathy in blood disorders - hyperviscosity

A

Diverse group of rare disorders characterised by increased blood viscosity due to polycytheamia or abnormal plasma protein

Polycrythaemia
- neoplastic proliferation of erythrocytes with increased bone marrow activity

Waldenstrom macroglobulinaemia
- is a malignant lympho-proliferation disorder with monoclonal IgM production

Ocular Features
-retinal haemorrhages and venous changes and occasional RVO

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42
Q

What is Age related macular degeneration

A
  • Degenerative disorder affecting the macula
  • clinical presentations of drusen and RPE changes in the absence of any other disorders
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43
Q

AMD Pathophysiology

A
  • RPE stops working properly with eventual loss of RPE
  • There is a breakdown of the blood retina barrier
  • BV’s from Bruch’s grow into the retina causing wet AMD
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44
Q

What Clinical assessments should be done for a Px with AMD

A
  • VA
  • Refraction
  • Cataract
  • Amsler - look for distortion on amsler grid
  • Dilated fundus examination
  • OCT if available
  • history
45
Q

AMD risk factors

A

Age
- major risk factor
- >90 y/o is most at risk

Race
- Caucasian most at risk

Hereditary
- 3x greater chance if Px has first degree relative

Smoking
Hypertension
Dietary factors

46
Q

What is drusen

A
  • Extracellular deposits located at the interface between the RPE and Bruch’s membrane
  • Composed of a broad range of constituents derived from immune mediated and metabolic processes
47
Q

Dry AMD

A
  • Gradual impairment of vision over months or years
  • Impairment of choroidal function due to age related changes, extracellular material builds up as it isn’t removed fast enough
48
Q

Dry AMD Symptoms

A
  • Gradual onset reduced vision, bilateral but asymmetric
  • Vision often better in bright light and may fluctuate
  • Metamorphopsia occurs in more advanced cases if lots of drusen (more common in wet AMD)
49
Q

Dry AMD Signs

A
  • numerous large soft drusen
  • hypopigmentation of RPE
  • enlargement of atrophied areas
  • drusenoid RPE detachment
50
Q

Dry AMD Management

A
  • monitor with amsler
  • consider nutritional supplements
  • optical aids
  • Non optical aids
  • minimise risk factors (smoking, diet, BP, alcohol consumption)
  • blind/partial sight registration
  • Vitamin C (Fruit and Veg)
  • Vitamin E (Seed oils, olive oil)
  • beta-carotene (vegetables)
  • zinc oxide (meat)
51
Q

Wet AMD Symptoms

A
  • Sudden onset reduced vision, generally unilateral
  • Metamorphopsia - esp at near
  • Positive scotoma - esp if extensive haemorrhage is present
52
Q

Wet AMD Management

A
  • Anti-VEGF injections
  • Laser (only in very specific situations)
  • Surgery (only in very specific situations)
53
Q

Which layer does the RPE detach from

A
  • RPE detaches from the inner collagenous layer of Bruch’s membrane
  • Due to disruption of the adhesion
54
Q

What is an Epiretinal membrane and types

A
  • This is a transparent, avascular, fibrocellular structure that develops over the surface of the retina
  • Proliferation and contraction of the membrane causes visual symptoms
  • Idiopathic or Secondary
55
Q

Idiopathic Epiretinal Membrane

A
  • No apparent cause, common aging process
  • Residual vitreous tissue remains on the retinal surface following cortical separation
56
Q

Secondary Epiretinal membrane

A
  • Occurs following retinal detachment surgery, retinal break, pan retinal photocoagulation and retinal vascular disease and inflammation
57
Q

Epiretinal Membrane signs

A
  • VA depends on severity
  • Irregular translucent sheen, best detected using green light
  • Macular puckering and vessel torsion
  • Distortion of BV’s
  • Macular Pseudohole
  • Retinal Telangiectasia
  • Distortions on amsler grid
  • Highly reflective surface on OCT
58
Q

Epiretinal Membrane treatment

A
  • Observation - when non progressive, VA may improve by itself, no need for referral if asymptomatic
  • Surgery - removal of the membrane via vitrectomy to facilitate peeling which usually improves vision by 2 lines
59
Q

What causes a Full thickness macular hole and who is most at risk

A
  • More common in females aged 60-70
  • Caused by vitroretinal traction
  • Can also be caused by high myopia and ocular trauma
60
Q

Macular hole signs

A
  • FTMH will cause impairment of central vision in one eye, first noticed when the fellow eye is occluded
  • Metamorphopsia
  • FTMH with red base and yellow white dots, surrounding grey cuff of subretinal fluid is usually present
  • VA of 6/60 for full thickness hole
  • May be accompanied by a PVD
61
Q

Macular Microhole

A

Full thickness defect that is smaller than 150um

62
Q

Macular hole treatment

A

Observation
- 50% of stage 1 holes heal following vitreous separation
- 10% of FT holes resolve themselves with improved VA

Pharmacological vitreolysis

Surgery
- stage 2 or greater
- vitrectomy
- 100% of holes get closed
- 90% experience improved VA of at least 6/12

63
Q

Lamellar macular hole

A
  • Partial thickness defect of the inner retina at the fovea
  • Intact photoreceptor layer
  • Develops from an anomalous PVD
64
Q

Vitreomacular adhesion

A
  • Residual attachment of the vitreous within a 3mm radius of the central macula in the presence of a vitreous separation
  • This is a stage in the process of a PVD
65
Q

Vitreomacular traction

A
  • Vitreous abnormally adherent to macula
  • The presence of retinal changes on the OCT with evident PVD
  • Distortion of the foveal surface
66
Q

What is Central Serous Retinopathy and who is most commonly affected

A
  • Localised serous detachment of the sensory retina at the macula, secondary to leakage from the choriocapillaris through on or more hyperpermiable sites on the RPE
  • Typically affects young/middle aged white men
  • Stress is a predisposing factor
67
Q

Central Serous Retinopathy signs

A
  • unilateral blurring
  • metamorphopsia
  • micropsia
  • dyschromatopsia
  • reduced VA
  • round/oval detachment of the sensory retina
  • chronic lesions associated with strophic change
  • eye can become more hyperopic
68
Q

Central Serous Retinopathy prognosis

A
  • spontaneous resolution after 3-6 months with return to near normal vision
  • recurrence seen 50% of the time
  • possible that it is chronic and lasts more than 12 months - this permanently reduces vision
69
Q

Central Serous Retinopathy management

A
  • Observation - appropriate in many cases
  • Oral sprionolactone
  • Laser - sub threshold diode laser of RPE site
  • Anti VEGF agents
70
Q

What is Cystoid Macular oedema

A
  • Results from the accumulation of fluid in the outer plexiform area and inner nuclear layer
  • formation of a tiny cyst
  • may develop into lamellar holes
  • retinal thickening at the macula due to disruption of normal blood retinal barrier
71
Q

Cystoid macular oedema causes

A
  • ocular surgery
  • retinal vascular disease
  • inflammation
  • drug induced
  • retinal dystrophies
  • Vitreomacular traction
72
Q

Cystoid Macular Oedema Signs

A

Symptoms
- blurring, distortion and micropsia

Signs
- loss of foveal depression
- thickening of the retina
- optic disc swelling
- lamellar hole

73
Q

Degenerative Myopia

A
  • progressive anteroposterior elongation of the sclera envelope associated with a range of secondary ocular changes
74
Q

Degenerative Myopia Signs

A

— pale appearance due to attenuation of the RPE
- large choroid vessels visible
- anomalous optic nerve head
- acquired optic disc pits
- lattice degeneration
- rhegmatogenous retinal detachment
- macular hole
- macular retinoschesis (retinal detachment without macular hole)
- peripapillary detachment
- cataract
- glaucoma
- amblyopia

75
Q

Angiod Streaks

A
  • crack like dehinsciences in brittle thickened and calcified bruchs membrane, associated with atrophy of the overlying RPE
76
Q

Angioid streaks Signs

A
  • gray or dark red linear lesions with irregular serrated edges that intercommunicate in a ring like fashion
  • optic disc drusen
  • scream depression is contraindicated in these eyes
77
Q

Choroidal folds

A
  • parallel grooves or striae involving the inner choroid
  • likely to develop in association with any process that indicates compressive stress within the choroid
  • primary mechanisms include choroidal congestion and and sclera compression
78
Q

Choroidal folds causes

A

Idiopathic
- may be present in healthy eyes
- hyperopia
- bilateral

Papilloedema
- elevated intracranial pressure

Orbital Disease
- retrobulbar tumours
- thyroid opthalmopathy

Ocular disease
- choroidal tumours
- inflammation
- retinal detachment
- posterior scleritis

79
Q

Choroidal Folds signs/symptoms

A

Symptoms
- variable affect on vision

Signs
- parallel lines at the posterior poles
- usually horizontal
- elevated portion of the fold is yellow and less pigmented

80
Q

Retinitis pigmentosa

A
  • clinical and general group of inherited diffuse retinal degenerative diseases, mainly affecting rod photoreceptors, and then later the cones
81
Q

Retinitis Pigmentosa Signs/symptoms

A

Symptoms
- dark adaptation difficulties
- peripheral visual problems (due to rod degeneration)
- reduced central vision is later than peripherally (as cones are affected last)

Signs
- pigment are changes and RPE atrophy
- increased density of pigment
- severe peripheral pigmentation
- anteriorlar narrowing and disc pallor
- optic disc drusen

82
Q

Retinitis Pigmentosa Complications

A
  • posterior subcapsular cataract
  • open angle glaucoma
  • keratoconous
  • PVD
83
Q

Retinitis Pigmentosa Treatment

A
  • follow up appointments
  • cataract surgery
  • low vision aids
  • avoid smoking
  • Vitimin A supplements
84
Q

Stargardt disease

A

Accumulation of of lipofuscin within the RPE

3 Types
- STGD1
- STGD3
- STGD4

85
Q

Stargardt Disease Signs/symptoms

A

Symptoms
- gradual impairment of central vision
- reduced colour vision
- impairment of dark adaption

Signs
- non specific mottling
- oval ‘snail slime’ appearance
- lesions at the level of the RPE

86
Q

Stargardt Disease Treatment

A
  • protection from high energy light exposure
  • Vitimin A supplements
  • gene therapy (ABCA4 gene)
87
Q

Juvenile Best Macular Dystrophy

A
  • due to allelic variation in the bestrophin gene
  • bestrophin is found on the plasma membrane of the RPE and functions as a transmembrane ion channel
  • vision worse’s as Px gets older
88
Q

Juvenile best macular dystrophy Diagnosis

A

Gradual evolution through the following stages
- pre-vitelliform is characterised by by a subnormal electrooculogram (EOG), with a normal fundus
- vitilliform. A round, sharply delineated macular lesion between half a disc and 2 disc diameters in size on the RPE
- pseudohypopyon may occur when part of the lesion regresses
- vitelliruptive. The lesion breaks up and visual acuity drops
- atrophic in which all pigment has disappeared, leaving an atrophic area of the RPE

89
Q

Tyrosine’s-negative oculocutaneous albinism

A
  • incapable of synthesising melanin
  • poor VA due to incomplete development
  • nystagmus
  • translucent iris
  • FUNDUS lacks pigment and choroidal vessels visible
90
Q

Tyrosine-positive oculocutaneous albinism

A
  • produce variable amounts of melanin
  • reduced VA
  • ## FUNDUS shows variable pigmentation
91
Q

Ocular Albinism

A
  • normal skin and hair, mainly ocular involvement
  • partial iris translucence
  • scattered areas of depigmentation and granularity
  • affected males have hypopigmentation iridis and fundi
92
Q

What is Posterior Vitreous Detachment and its risk factors

A
  • separation of the cortical vitreous along with the posterior hyaloid membrane
  • PVD occurs due to vitreous gel liquification with age to form fluid filled captives
  • age is the biggest risk factor of PVD, along with cataract surgery, trauma, uveitis and panretinal photocoagulation
93
Q

PVD Diagnosis

A

Symptoms
- flashing lights (transient flashes of light in the periphery, brought on by eye/head movement)
- floaters (Weiss ring)
- blurred vision

Signs
- detached PHM can often be viewed
- Haemorrhage may be indicated by blood in the anterior vitreous
- pigment granules in the anterior vitreous
- retinal breaks

94
Q

PVD Effects

A
  • PVD reduces risk of macular hole formation and eliminates risk of proliferative DR
  • minority of px’s with a symptomatic vitreous separation develop a retinal tear, progress to RD if untreated
95
Q

PVD Management

A
  • Px should be examined as soon as possible, especially if myopic or have a family history of RD
  • assess the risk of RD, number of floaters, haemorrhaging etc
  • if Px is of a high risk of RD they should be reviewed more regularly
96
Q

How do Retinal breaks form

A
  • result due to traction at sites of vitreoretinal adhesion
  • breaks usually occur at or soon after the onset of PVD symptoms
97
Q

What is a horseshoe tear

A
  • Consists of a lap, whose apex is being pulled anteriorly by the vitreous, while the base remains attached to the retina
98
Q

Detecting Retinal Tears - what is schafers sign

A
  • Schafer’s sign - presence of pigment in anterior vitreous
  • If retina tears, RPE cells exposed and migrate into vitreous - visible as pigmented specks
  • Absence of Schafer’s sign does not exclude a retinal break
99
Q

What are Retinal holes and how do they occur

A
  • round or oval and smaller than tears
  • may occur in lattice degeneration
100
Q

Management of retinal breaks

A
  • Px should be advised of the symptoms of a PVD and RD and supplemented with written information
  • retinal breaks without RD can be treated with laser or cryotherapy
101
Q

Rhegmatogenous Retinal Detachment

A
  • characterised by a retinal detachment in concert with vitreoretinal traction, that allows liquefied vitreous under the sensory retina, separating it from the RPE
102
Q

Symptoms of Rhegmatogenous RD

A
  • flashing lights and floaters
  • curtain forming over peripheral vision
  • lower visual field defects
103
Q

Signs of Rhegmatogenous RD

A
  • RAPD
  • lower IOP
  • iriditis, may even cause posterior syneachiae
  • tobacco dust consisting of pigment cells is commonly seen in the anterior chamber
  • retinal breaks appear as discontinuities in the retinal surface and are usually red
104
Q

Tractional Retinal Detachment

A
  • caused by proliferative retinopathy
  • contraction of fibrovascular membranes
105
Q

Tractional Retinal Detachment - Signs & Symptoms

A

Symptoms
- slowly progressing VF defect

Signs
- RD has a concave configuration and breaks are absent
- retinal mobility is severely reduced
- if a break occurs in a tractional RD it assumes the characteristics of a Rhegmatogenous RD and progresses rapidly

106
Q

Exudative Retinal Detachment

A

Accumulation of sub-retinal fluid in the absence of retinal breaks or traction caused by:
- choroidal tumours
- inflammation
- bulbous central serous chorioretinopathy
- choroidal neovascularisation
- hypertensive choroidopaty.
- idiopathic

107
Q

Exudative RD - Symptoms

A
  • bilateral
  • floaters
  • sudden visual defect
108
Q

Exudative RD - Signs

A
  • RD has convex configuration
  • detached retina is very mobile due to the phenomenon of shifting fluid
  • Leopard spots consisting of scattered areas of subretinal pigment clumping
109
Q

Vitrectomy

A
  • vitreous is replaced with another liquid
  • cannula is inserted at the level of the inferior border of the lateral Rectus
  • central vitreous gel and posterior hyaloid face are excised
  • surgical techniques involve delamination and segmentation

Clinical Opthalmology (7 decks)

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