macula and choroid Flashcards

1
Q

what are maculopathies ?

A

conditions that affect the macula and the choroid

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2
Q

what are the different types of maculopathies ?

A
  • acquired

- hereditary

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3
Q

what are hereditary conditions ?

A
  • macular dystrophies
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4
Q

what are acquired conditions ?

A
  • AMD
  • central serous retinopathy (CSR)
  • macular hole
  • cystoid macula oedema (CMO)
  • myopic maculopathy
  • choroidal neovascularisation
  • epiretinal membrane (ERM)
  • diabetic maculopathy
  • drug-induced maculopathies
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5
Q

what are the symptoms common to all maculopathies ?

A

. reduced vision especially at near

. positive scotoma - smudge or a visible blur at centre of vision

. distortion ( metamorphopisa)
- complain that straight lines appear wobbly or that door frames look crooked

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6
Q

what are rare symptoms of maculopathies?

A
- micropsia (rare)
. increased spacing of foveal cones 
e.g.  caused space occupying lesion 
- macropsia (rare)
. reduced spacing of foveal cones
e.g.  caused oedema 

. the patient will complain of distortion in central vision

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7
Q

what investigation to carry for diagnosis for maculopathies ?

A
  1. BCVA
    - near vision both monocularly and binocularly
  2. Amsler grid - to record and measure distortion
  3. pupils light reaction
    - expect to be normal
    - differentiates from optic nerve lesions
  4. dilated fundus examination using SL-BIO which helps look at subtle changes
  5. OCT - visualise the inner layer
  6. fundus autofluorescence
  7. HES- fluoroscein angiography
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8
Q

what are the characteristics of fundus autofluorescence imaging ?

A

. blood vessels are fluorescing

. optic nerve head is fluorescing

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9
Q

what are the characteristics of fluorescein angiography ?

A

. fluorescein is injected to a vein and the fluorescein flows around the vasculature and series of photographs are taken and blood vessels are filled with fluorescence

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10
Q

what is central serous retinopathy (CSR)?

A
  • a type of maculopathy
  • also called central serous choroidal retinopathy
  • exudative detachment of sensory retina in macula area
  • subtle pigmentary changes and shallow area of sub-retinal fluid
  • common cause of centra vision loss ( 4th most common retinopathy after AMD, DR and RVO)
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11
Q

what is the pathogenesis of central serous retinopathy ?

A
  • poorly understood
  • due to multiple leaks in extrafoveal RPE
    . FA ‘’ smoke stack’’ or ‘‘ink blot’’ appearance
    . active choroidal leakage
    -ICG
  • impaired choroidal circulation
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12
Q

what is the epidemiology of central serous retinopathy ?

A
. incidence 10 per 100,000 in M
. M to F 6:1 to 10:1 ratio
. 25-50 year age group
. unilateral (80%)
. 30% recur
- in ipsilateral or contralateral eye
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13
Q

what are the risk factors of central serous retinopathy ?

A

. type A personality
. elevated testosterone levels
. systemic steroid use

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14
Q

what are the symptoms of central serous retinopathy ?

A

. sudden onset reduced VA/blurring

  • VA 6/9 to 6/18
  • possible hyperopic shift due to elevation of retina

. positive scotoma - interruption to central vision
. metamorphopsia- distortion
. micropsia

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15
Q

what is the clincal presentation of acute central serous retinopathy ?

A
.detachment of sensory retina with serous fluid between RPE and photoreceptor outer segs
- oval/round elevation
- shallow
. absent/attenuated foveal reflex
. pigment changes
. PED

. 30% Px will have recurrence within a year
. multiple recurrence lead to chronic central serous retinopathy

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16
Q

what is the clinical presentation of chronic central serous retinopathy ?

A

. RPE atrophy

. risk of CNV

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17
Q

how to differentiate between chronic CSCR and wet AMD?

A
  • patients with CSCR are younger than patients with wet AMD
  • CSR resolves on its own accord
  • wet AMD progresses
  • differentiation with wet AMD based on age of onset and progression
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18
Q

what is the optometric management of CSR ?

A
. reassure patient
. CSR tends to resolve spontaneously within 2-3 months
. VA recovers approx 90% of patients
. subtle metamorphopsia may persist
. refer to ophthalmologist
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19
Q

what is the ophthalmological management of CSR ?

A
. confirmation of diagnosis
. observation
. tapering of systemic steroids
. PDT or focal laser 
- hastens resolution but does not affect visual outcome
. Anti-VEGF?
. guarded prognosis if recurrent/chronic
20
Q

what are the different types of macular holes dependent on ?

A
  • refers to extent of retina that is involved
21
Q

what is a full thickness macular hole?

A
  • this is a hole that goes from the internal limiting membrane all the way through to the RPE
22
Q

what are the clinical features of full thickness macular hole?

A

. edge of hole

  • pseudocysts ( small intra retinal spaced )
  • edge of fovea is thickerthan normal

. ‘punched out’ circle appearance at macula

. pseudocysts at edge

. pigment changes at base of hole

. edges may appear sl.raised

23
Q

what is partial thickness macular hole or lamellar macular hole?

A
  • photoreceptors are intact
  • loss of layers of retina
  • irregular foveal contour
  • retinal cells are still attached to the posterior vitreous face known as operculum
24
Q

what is an operculum ?

A

retinal cells are still attached to the posterior vitreous face known as operculum

25
Q

what are the causes of macular hole ?

A
  1. traction
    - this is where retina is lifted from RPE pump
    - causes macular oedema
  2. idiopathic
  3. trauma to eye
  4. inflammation
26
Q

what is the prevalence of macular hole ?

A

. 1 in 3,300
. 6th and 7th decades
. typically female
. bilateral in 10-30% of cases

27
Q

what are the symptoms of macular hole ?

A
  • painless loss of vision
  • full thickness macular hole the VA is 6/60
  • partial macular hole vision may be better
  • positive scotoma
  • metamorphopsia
28
Q

what is the treatment of macular hole ?

A

. self resolving - no treatment required
. not urgent referral
. put px under observation
. new full thickness macular may require surgery

29
Q

how is the surgery of macular hole carried out ?

A
  • vitrectomy and peel
  • post-operative positioning - sitting with face down to allow retina to adhere
  • visual outcome depends on presenting VA
  • risk of cataract
30
Q

what is cystoid macular oedema ?

A
  • cystoid macular oedema causes a painless loss of central vision (6/12-6/60)
  • result of fluid accumulation ( cysts ) at OPL and INL of fovea
  • fluid accumulation is a result of breakdown of blood-retinal barrier
31
Q

what is the short term result of cystoid macular oedema ?

A
  • may not be serious

- can improve without treatment

32
Q

what happens if cystoid macular oedema becomes chronic or severe ?

A
  • can be difficult to treat
  • may cause permanent drop in central vision
  • cysts may coalesce/merge to form a lamellar hole
33
Q

what are the clinical signs of cystoid macular oedema ?

A
  • loss of foveal depression
  • cysts may be visible with an OCT- appear as hyporeflective ( dark ) spaces within the retina
  • FA ( fluorescein angiography ) typical ‘flower-patel’ pattern of late hyperfluorescence ( due to dye accumulation with time in the OPL cysts )
34
Q

what are the causes of cystoid macular oedema ?

A
  • post surgery
  • diabetes
  • wet AMD - fluid leakage from the blood vessels results in cystic spaces being formed can cause cystoid macular oedema
  • retinal vein occlusion
  • uveitis
  • epiretinal membran
  • radiation retinopathy
  • choroidal tumours
  • retinitis pigmentosa
  • prostaglandin analogue eyedrops for glaucoma
  • macula telangectasia
  • coats disease
35
Q

what is irvine-gass syndrome ?

A
  • it is cystoid macular oedema which follows cataract surgery
  • occurs 1-3 months post-op
  • clinically significant CMO affects 10% after routine cataract surgery ( but 25-40% show CMO on FA)
36
Q

what happens when a patient has cataract surgery ?

A
  • they are invited to an appointment 6-12 weeks after surgery, during which they have an OCT to identify if there is any element of cystoid macular oedema
37
Q

what happens to diabetic patients post-cataract surgery ?

A
  • in diabetes, post-cataract surgery CMO occurs in 32% without DR ( diabetic retinopathy ) , and 81% of diabetics with DR
  • pre-existing diabetic macular oedema should be treated before cataract surgery whenever possible
38
Q

what is the treatment of Irvine-gass syndrome ?

A
  • topical non-steroidal anti-inflammatory drugs (NSAIDs)
  • topical corticosteroids
  • anti-VEGF
39
Q

what does pathological/degenerative myopia cause ?

A
  • degenerative changes in sclera, choroid and RPE
  • > -6D
  • AL ( axial length) greater than 26mm
  • significant cause of visual impairment in working population
40
Q

how prevalent is pathological/degenerative myopia ?

A
  • 2 to 10% population

- race dependent

41
Q

what are the systemic associations of high myopia ?

A

. down syndrome
. marfan syndrome
. prematurity
. ehlers-danlos syndrome

42
Q

how does myopic fundus look like ?

A
  1. pale tessellated ( tigroid) fundus
    - diffuse attenuation of RPE ( RPE is thinned ) with increased visibility of choroidal vasculature
  2. focal chorioretinal atrophy
    - patchy areas where choroid ( and possibly ) sclera visible due to elongation of globe
  3. anomalous optic nerve head
    - small, large or tilted appearance ( edges more blurred on one side )
  4. peripapillary chorioretinal atrophy
    - atrophy surrounding optic nerve head
    - common
    - includes peripapillary intrachoroidal cavitation = small yellow-orange area inferior to disc
    - can cause visual field defect
  5. acquired optic disc pit
    - due to expansion of peripapillary area over time
  6. Lacquer cracks
  7. subretinal haemorrhages ( may develop from lacquer cracks )
  8. choroidal neovascularisation
  9. Fuch’s spot
43
Q

what are lacquer cracks ?

A

. linear breaks in RPE-bruch’s membrane complex

  • fine yellowe lines, criss-crossing
  • stretching and degeneration of the choroid from elongation of globe
  • associated with CNV( choroidal neovascularisation ) in 82% of eyes
44
Q

what is the prevalence of choroidal neovascularisation ( CNV) ?

A

. CNV in 10% highly myopic eyes

  • CNV located between neurosensory retina and RPE
  • minimal sensory retinal elevation

. typical onset 40-50 years

. better prognosis than with CNV in AMD

. location is mostly subfoveal in 60%
. juxtafoveal ( to the side ) in 30%

45
Q

what does myopic CNV lead to in the advanced stages ?

A

. advanced stages: leads to Fuch’s spot

  • macular scar with pigment clumping
  • raised, follows reabsorption of sub retinal bleed
  • treatment : anti-VEGF
46
Q

what other changes that can occur in myopic eye ?

A

. staphyloma
- peripapillary or macular ectasia of posterior sclera due to focal thinning

. lattice degeneration
. retinal tears and breaks
. retinal detachment

. macular retinoschisis
- possible in eyes with staphyloma due to macular traction

. macular hole
- spontaneous or after trauma

47
Q

what are other myopia complications ?

A

. premature lenticular opacities
- PSC or early onset nuclear sclerosis

. lens dislocation - may be associated with systemic conditions

. primary open angle glaucoma
- increased prevalence