Retina Flashcards
1
Q
Risk factors of diabetic retinopathy
A
- duration of diabetes
- poor control of diabetes
- pregnancy
- hypertension
- nephropathy
2
Q
DR Pathogenesis
A
- microangiopathy in which small BV’s are vulnerable due to high glucose levels
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)
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
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
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
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
8
Q
Retinal Vein Occlusion Risk Factors
A
- age
- hypertension
- hyperlipidaemia
- diabetes
- glaucoma
- OCP
- smoking
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
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
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
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
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
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
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
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
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
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
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
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
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
22
Q
Ocular Ischemic Syndrome
A
- results from chronic ocular hypoperfusion (reduced blood flow), secondary to severe ipsilateral carotid stenosis
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
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
25
Types of Hypertensive eye disease
- Retinopathy
- Choroidopathy
26
Hypertensive Eye Disease - Retinopathy grading system
- 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
27
Hypertensive retinopathy prognosis
- 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
28
Hypertensive Retinopathy Management
- Grade 1+2 - referral to GP for BP check
- focus on reducing blood pressure
29
Hypertensive Eye Disease - Choroidopathy
- 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
30
Sickle cell Retinopathy
- Caused by abnormal haemoglobins that induce RBC to adopt an anomalous shape under conditions of physiological stress such as hypoxia (low levels of oxygen)
31
Sickle cell Retinopathy - Non Proliferative Retinopathy
- 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
32
Sickle cell Retinopathy - Proliferative Retinopathy
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
33
Sickle Cell Retinopathy - Management
- 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
34
Retinopathy of Prematurity
- 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
35
Stages of Retinopathy of Prematurity
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
36
Retinopathy of prematurity treatment
- cryotherapy
- anti VEGF agents
- Pars plana vitrectomy
37
Primary Retinal Telangiectasia
Develops secondary to vascular compromise
Comprises a group oof rare, idiopathic, congenital or acquired retinal vascular anomalies characterised by dilation and tortuosity
38
Retinopathy in blood disorders
- Leukaemia
- Anaemia
- Hyperviscosity
39
Retinopathy in blood disorders - Leukaemia and its major variants and signs
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
40
Retinopathy in blood disorders - anaemia
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
41
Retinopathy in blood disorders - hyperviscosity
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
42
What is Age related macular degeneration
- Degenerative disorder affecting the macula
- clinical presentations of drusen and RPE changes in the absence of any other disorders
43
AMD Pathophysiology
- 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
44
What Clinical assessments should be done for a Px with AMD
- VA
- Refraction
- Cataract
- Amsler - look for distortion on amsler grid
- Dilated fundus examination
- OCT if available
- history
45
AMD risk factors
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
What is drusen
- 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
Dry AMD
- 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
Dry AMD Symptoms
- 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
Dry AMD Signs
- numerous large soft drusen
- hypopigmentation of RPE
- enlargement of atrophied areas
- drusenoid RPE detachment
50
Dry AMD Management
- 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
Wet AMD Symptoms
- Sudden onset reduced vision, generally unilateral
- Metamorphopsia - esp at near
- Positive scotoma - esp if extensive haemorrhage is present
52
Wet AMD Management
- Anti-VEGF injections
- Laser (only in very specific situations)
- Surgery (only in very specific situations)
53
Which layer does the RPE detach from
- RPE detaches from the inner collagenous layer of Bruch's membrane
- Due to disruption of the adhesion
54
What is an Epiretinal membrane and types
- 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
Idiopathic Epiretinal Membrane
- No apparent cause, common aging process
- Residual vitreous tissue remains on the retinal surface following cortical separation
56
Secondary Epiretinal membrane
- Occurs following retinal detachment surgery, retinal break, pan retinal photocoagulation and retinal vascular disease and inflammation
57
Epiretinal Membrane signs
- 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
Epiretinal Membrane treatment
- 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
What causes a Full thickness macular hole and who is most at risk
- More common in females aged 60-70
- Caused by vitroretinal traction
- Can also be caused by high myopia and ocular trauma
60
Macular hole signs
- 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
Macular Microhole
Full thickness defect that is smaller than 150um
62
Macular hole treatment
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
Lamellar macular hole
- Partial thickness defect of the inner retina at the fovea
- Intact photoreceptor layer
- Develops from an anomalous PVD
64
Vitreomacular adhesion
- 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
Vitreomacular traction
- Vitreous abnormally adherent to macula
- The presence of retinal changes on the OCT with evident PVD
- Distortion of the foveal surface
66
What is Central Serous Retinopathy and who is most commonly affected
- 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
Central Serous Retinopathy signs
- 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
Central Serous Retinopathy prognosis
- 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
Central Serous Retinopathy management
- Observation - appropriate in many cases
- Oral sprionolactone
- Laser - sub threshold diode laser of RPE site
- Anti VEGF agents
70
What is Cystoid Macular oedema
- 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
Cystoid macular oedema causes
- ocular surgery
- retinal vascular disease
- inflammation
- drug induced
- retinal dystrophies
- Vitreomacular traction
72
Cystoid Macular Oedema Signs
Symptoms
- blurring, distortion and micropsia
Signs
- loss of foveal depression
- thickening of the retina
- optic disc swelling
- lamellar hole
73
Degenerative Myopia
- progressive anteroposterior elongation of the sclera envelope associated with a range of secondary ocular changes
74
Degenerative Myopia Signs
— 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
Angiod Streaks
- crack like dehinsciences in brittle thickened and calcified bruchs membrane, associated with atrophy of the overlying RPE
76
Angioid streaks Signs
- 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
Choroidal folds
- 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
Choroidal folds causes
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
Choroidal Folds signs/symptoms
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
Retinitis pigmentosa
- clinical and general group of inherited diffuse retinal degenerative diseases, mainly affecting rod photoreceptors, and then later the cones
81
Retinitis Pigmentosa Signs/symptoms
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
Retinitis Pigmentosa Complications
- posterior subcapsular cataract
- open angle glaucoma
- keratoconous
- PVD
83
Retinitis Pigmentosa Treatment
- follow up appointments
- cataract surgery
- low vision aids
- avoid smoking
- Vitimin A supplements
84
Stargardt disease
Accumulation of of lipofuscin within the RPE
3 Types
- STGD1
- STGD3
- STGD4
85
Stargardt Disease Signs/symptoms
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
Stargardt Disease Treatment
- protection from high energy light exposure
- Vitimin A supplements
- gene therapy (ABCA4 gene)
87
Juvenile Best Macular Dystrophy
- 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
Juvenile best macular dystrophy Diagnosis
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
Tyrosine’s-negative oculocutaneous albinism
- incapable of synthesising melanin
- poor VA due to incomplete development
- nystagmus
- translucent iris
- FUNDUS lacks pigment and choroidal vessels visible
90
Tyrosine-positive oculocutaneous albinism
- produce variable amounts of melanin
- reduced VA
- FUNDUS shows variable pigmentation
-
91
Ocular Albinism
- normal skin and hair, mainly ocular involvement
- partial iris translucence
- scattered areas of depigmentation and granularity
- affected males have hypopigmentation iridis and fundi
92
What is Posterior Vitreous Detachment and its risk factors
- 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
PVD Diagnosis
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
PVD Effects
- 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
PVD Management
- 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
How do Retinal breaks form
- result due to traction at sites of vitreoretinal adhesion
- breaks usually occur at or soon after the onset of PVD symptoms
97
What is a horseshoe tear
- Consists of a lap, whose apex is being pulled anteriorly by the vitreous, while the base remains attached to the retina
98
Detecting Retinal Tears - what is schafers sign
- 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
What are Retinal holes and how do they occur
- round or oval and smaller than tears
- may occur in lattice degeneration
100
Management of retinal breaks
- 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
Rhegmatogenous Retinal Detachment
- characterised by a retinal detachment in concert with vitreoretinal traction, that allows liquefied vitreous under the sensory retina, separating it from the RPE
102
Symptoms of Rhegmatogenous RD
- flashing lights and floaters
- curtain forming over peripheral vision
- lower visual field defects
103
Signs of Rhegmatogenous RD
- 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
Tractional Retinal Detachment
- caused by proliferative retinopathy
- contraction of fibrovascular membranes
105
Tractional Retinal Detachment - Signs & Symptoms
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
Exudative Retinal Detachment
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
Exudative RD - Symptoms
- bilateral
- floaters
- sudden visual defect
108
Exudative RD - Signs
- 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
Vitrectomy
- 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
