tHIS talk gives information about white dot syndromes the clinical features, how to differentiate them treatment etc

1. White Dot syndromes
-For Ophthalmology PGs
Dr. Vivek B Wani MS FRCSEd
Consultant Vitreoretina Surgeon
KLES Dr.Prabhakar Kore Hospital
Belagavi
1

2. What are White Dot
Syndromes(WDS)?
• White dot syndromes are a group of
inflammatory chorioretinopathies
characterized by
the presence of multiple white/yellow lesions
located at outer retina, RPE, choriocapillaris,
and choroid
associated with variable inflammation in
anterior segment and vitreous
usually affect young female myopes
2

3. WDS other common features
• They have common presenting symptoms like
photopsias, blurred vision, floaters, and visual
field loss
• Many syndromes are preceded by a viral
prodrome
• Most are bilateral and affect F>M (MEWDS is
unilateral and AMPPE IS M=F)
• The etiology of white dot syndromes remains
unknown -possible causes include
autoimmune/inflammatory, viral infection,
genetic predisposition, parasitic infection
3

4. Which conditions are included in
WDS?
Though there are some controversies the following are
commonly included in this group
1. Multiple evanescent white dot syndrome(MEWDS)
2. Acute Posterior Multifocal Placoid Pigment
epitheliopathy(AMPPE)
3. Multifocal Choroiditis & Panuveitis (MCP)
4. Acute Zonal Occult Outer Retinopathy(AZOOR)
5. Acute Macular Retinopathy
6. Birdshot Retinochoroidopathy (BRC)
7. Serpigenous choroidopathy
8. Punctate Inner choroidopathy (PIC)
4

5. 5
1. Multiple Evanescent White Dot
syndrome (MEWDS)
MEWDS is Unilateral (most WDS are bilateral)
rarely bilateral
• F>M 5:1, 20-50 years, moderate myopes
C/O- Blurred vision, shimmering photopsia,
dyschromatopsia, paracentral and temporal
scotoma
• Prodromal viral infection common in
50%

6. MEWDS-clinical features
• VA 20/20 TO 20/400
• MILD RAPD+
• AC clear
• Vitritis mild, disc edema +/-
• Multiple small white/yellowish lesions at outer retina and RPE are
seen distributed in perimacular area and up to the mid-periphery
• Fovea shows typical orange granularity
• Spots disappear over 1-2 months but foveal granularity may remain
• Vision recovers usually by 10 weeks
• Some photopsia , enlargement of blind spot and dyschromatopsia
may persist
• Some may show recurrence
• Very rarely CNV may develop as late complication
6

7. 7
• VA 20/20 TO 20/400
• MILD RAPD+
• AC clear
Anterior
segment
• Vitritis mild, disc edema +/-
• Multiple small white/yellowish lesions at outer
retina and RPE are seen distributed in
perimacular area and up to the mid-periphery
• Fovea shows typical orange granularity
Fundus
• Spots disappear over 1-2 months but foveal
granularity may remain
• Vision recovers usually by 10 weeks but
photopsia , enlargement of blind spot and
dyschromatopsia may persist
• Some may show recurrence & rarely CNV
Further
changes

8. 8
• Lesions and ONH -hypefluorescent
• Spots seen arranged in wreath like fashion on
FFA
• ICG angio -hypofluorescence over the spots and
may reveal more spots than seen clinically
FFA
ICG
• Enlarged blindspot and temporal field defect
• OCT-disruption of ellipsoid zone, hypereflective
material between RPE and neurosensory retina
that extends in to interdigitation zone, ellipsoid
zone and outer nuclear layer area
ICG
Visual field
OCT
• FAF-the spots are hyperreflective,
granularity in fovea is hypo fluorescent
• ERG- shows depressed ‘a’ wave
FAF
ERG

9. Investigations
• FFA shows hyperfl spots, disc hypefluorescent
• May be arranged in wreath like fashion
• ICG angio -hypofluorescence over the spots and may reveal
more spots than seen clinically
• VF –enlarged blind spot, temporal field defects
• OCT-disruption of ellipsoid zone, hypereflective material
between RPE and neurosensory retina that extends in to
interdigitation zone, ellipsoid zone and outer nuclear layer
area
• FAF-the spots are hyperreflective, granularity in fovea is
hypo fluorescent
• ERG- shows depressed a wave
9

10. Treatment
• Usually self limiting
• Recurrence in 10% may be treated with
immune modifying agent like cyclosporine
• Acute idiopathic blind spot enlargement
syndrome is considered same as MEWDS
• Anti VEGF inj if CNV occurs
10

11. From Kanski
11

12. MEWDS PIC From Quillen et al AJO 2004
12

13. MEWDS FFA AND OCT From Raven et al
13

14. MEWDS FFA AND ICG From kanski
14

15. MEWDS-DON’T FORGET FIVE POINTS
• Unilateral 90% , F>M 5:1
• C/o –DV, photopsia shimmering, field defects
• Fundus-vitritis +, disc hyperemia/edema, white
spots around disc and midperiphery, Foveal
granularity
• FFA –hyperfl spots, OCT- hyperreflective material
in interdigitation zone & EZ, Visual field -enlarged
blind spot
• Self limiting recovers by 10 weeks good
prognosis
15

16. Acute Posterior Multifocal Placoid
Pigment epitheliopathy (APMPPE)
• Bilateral but may not be simultaneous – Few weeks interval between the 2 eyes
• 20-30 years, F=M
• Prodromal viral illness in 1/3, meningeal complaints in few( careful), after
vaccination for influenza, varicella and hepatitis and after mumps or sarcoidosis
• C/O Visual impairment in one eye, other eye involved by 1-4 weeks, and field
defects
• AC quiet, Vitreous cells few
• Posterior pole shows multiple cream colored placoid lesions of <1 DD size at outer
retina, RPE and choriocapillaris level . No serous or exudative RD like in VKH
• Lesions start fading rapidly by ten days to month starting with central part of the
lesion and may leave variable pigmentary changes
• It is considered as delayed type hypersensitivity reaction of Type IV mediated by T
lymphocytes
• DD-sarcoidosis, tuberculosis VKH
16

17. APMPPE- investigations
• FFA- Typical early hypofluorescence followed by
hypeflourescence of the lesions
• OCT- hyperreflectivity of the outer retinal layers which
resolves slowly, ellipsoid disruption
• FAF-appear hypofluorescent and the number lesions
appear less than in FFA
• ICG the lesions remain hypoflurescent(hypocyinent)
through out the ICG
• If CNS symptoms like headache present do NEURO
CONSULT AND MRI
• Cerebral vasculitis with APMPPE can cause stroke
17

18. Treatment
• Usually resolve on their own to have VA of 20/40
or better
• Recurrences are rare
• Poor prognosis when
 pt is of old age
unilateral disease
foveal involvement by lesions
recurrences
• Steroids may help if started early in such poor
prognosis cases
18

19. From Quellen et al AJO 2004
19

20. FROM KANSKI TEXT BOOK
20

21. From Burke et al Eye. 2017; 31(10): 1399–1408. see the next slide for explanation 21

22. Evolution of lesions in phase 2 (right eye of Patient 3). One lesion is
identified with a red circle. It is hypofluorescent in the early phase of
the FFA (a) with late hyperfluorescence (b),
ICGA- but persistent hypocyanescence across all frames (c, d) on
ICGA.
OCT-A revealed an absence of flow signal (e1) at the level of the
choriocapillaris that progressively improved during follow-up (e2, e3).
The en face-OCT confirms that the decrease in flow at the level of the
choriocapillaris is not a consequence of signal attenuation secondary
to hyper-reflectivity of overlaying lesions (f).
Similarly in horizontal (g) and vertical (h) sections of the SD-OCT
through the lesion (red and green arrows, respectively) demonstrate
that the findings evolve from an initial hyper-reflectivity at the level of
the outer retina (g1, h1) to a progressive retinal thinning with
disruption of the RPE layer (g2, 3 and h2, 3).
On FAF (i) lesions evolved from predominant hypoautofluorescence
(i1) at baseline to central hyperautofluorescence (i2), but this
subsequently gave way to a recurrence of hypoautofluorescence (i3).
A full color version of this figure is available at the Eye journal online.
22

23. APMPPE Don’t forget five points
• Bilateral, M=F, young patients, viral prodrome C/O DV, field
defects, No AC activity, few vitreous cells, disc edema may
be
• Cream colored multiple plaque like lesions over the
posterior pole at outer retina and RPE level and may extend
beyond arcades. Lesions are larger than MEWDS
• FFA early hypo and later hyperfl, ICG-hypo throughout the
angio, OCT angio shows filling defects in choriocapillaris
• Self limiting, most resolve to have some RPE changes and
good VA 20/40 or better
• Unilateral cases, old age, foveal involvement can have
poorer outcome and may need systemic steroids. Keep in
mind the association of cerebral vasculitis!
23

24. Multifocal Choroiditis & Panuveitis
(MCP)
• Bilateral, F>M, 3rd to 4th decades, myopic patients and
bilateral but asymmetric
• C/O DV, floaters, photopsias and field defects
• Fundus- anterior chamber cells+, vitritis+, disc hyperemic,
cystoid macular edema, retinal vasculitis
• Fresh lesions are yellowish white lesions at outer retina and
RPE level,
• Most old lesions are 50-100 mu, well demarcated, punched
out chorioretinal scars with pigmented borders, vitritis+
and spread over posterior pole and periphery
• Chronic course with repeated exacerbations with poor
prognosis
• Patients lose vision due to lesions in fovea, CME, CNV
24

25. MCP
• MCP and presumed ocular histoplasmosis are
differentiated by presence of vitritis in MCP
• Some feel PIC, MCP are in the same spectrum
PIC also has no or less vitritis
• Cause is not known
25

26. Investigations
• FFA- the acute lesions show hypofl in early phase then
show hyperfluorescence
• CME, CNV may be present on FFA
• OCT shows hyperreflective drusen like material beneath
RPE
• FAF –shows many hypoflourescent spots in posterior pole
and periphery
• ICG-shows hypocyanescent spots in excess of those seen
with ophthalmoscopy
• ERG- shows depressed a and b waves
• Field defects- enlarged blind spot and peripheral defects
26

27. Treatment
• Systemic steroids, periocular steroids, topical
steroids depending upon the stage of the
disease
• Early treatment and proper monitoring may
help preserve vision
• Some times immune modulating agents may
be used
• CNV may need anti VEGF injection
27

28. Five points to remember MCP
• 3rd to 4 th decades, F>M, Bilateral, myopes
Present with DV, photopsia and floaters
• Anterior uveitis, vitritis, multiple choroiditis lesions,
initially whitish later punched out lesions with
pigmented borders, CME, foveal scarring, CNV
• FFA shows lesions to be initially hypofl and later
hyperfl, VF-field defects, ERG suppressed
• Treatment oral steroids and topical and periocular
steroids
• Prognosis guarded for vision
28

29. MCP
29

30. Knickelbein et J Clin Exp Ophthalmol .2016;7(3): 570
legend for the previous slide
• Multimodal imaging of a 29 year-old woman with multifocal choroiditis
and panuveitis (MCP).
• Color fundus photography (Color) demonstrates round chorioretinal
lesions of various size scattered throughout the macula and periphery.
• On fundus autofluorescence (FAF), some lesions were
hypoautofluorescent (likely atrophic), some mixed hyper- and hypo-
autofluorescent, and some had a surrounding hyperautofluorescent halo
(likely active).
• Fluorescein angiography (FA) showed early hypofluorescence (not shown)
with late staining (Late FA).
• On indocyanine green angiography (ICGA), lesions were hypofluorescent
early (Early ICGA) with persistence and expansion of hypofluorescence in
late frames (Late ICGA).
• Optical coherence tomography (OCT) showed hyper-reflective outer
retinal nodular lesions corresponding to clinically apparent lesions with
more widespread disruption in the surrounding outer retinal architecture.
30

31. Acute Zonal Occult Outer
Retinopathy(AZOOR)
• AZOOR is a syndrome of one or more episodes of outer
retinal dysfunction that occurs in young to middle age
patients, F>>M, myopes
• Unilateral initially but the other eye is involved in 75%
• Patients present initially with photopsia, field defect
with specific complaint of moving colors in the area of
field defect
• Gass includes in the category of AZOOR group of
disorders-- AZOOR, idiopathic blind spot enlargement
syndrome, MEWDS, Acute macular neuroretinopathy,
and multifocal choroiditis (MCP)
31

32. AZOOR clinical features
• No AC reaction
• RAPD+
• Early cases may be missed bcs Initially no fundus features
• vitritis + sometimes subtle RPE changes are present especially around the
disc –peripapillary RPE atrophy
• Visual field defect usually temporal later enlarges and moves centrally or
peripherally-when bilateral it may be confused as bitemporal hemianopia
• Later the RPE develops pigmentary changes, pigmentary clumps in the
area of field defect and may resemble RP, with vascular attenuation too
• AZOOR is outer retinal dysfunction
• 1/3 develop recurrence with growing edge of lesion forming grey
intraretinal lesions and the condition is sometimes named acute annular
outer retinopathy
32

33. Investigations
• FFA initially normal may show RPE window
defect where RPE is affected
• OCT- shows disappearance of ellipsoid zone
and outer segments in the involved area
• ERG shows outer retinal dysfunction with ‘a’
wave depression
• See the figure in the next slides
33

34. Pathology and prognosis
• Viral infection of RPE is supposed to cause
immune reaction leading to the changes
• In 1/3 of cases AZOOR recurs and may become
chronic
• 80% get stabilized visual field and recovery of
visual field in 20%
• Photopsias may last long
• No known treatment but steroids and
immunosuppressive have been tried
34

35. Knickelbein et J Clin Exp Ophthalmol .2016;7(3): 570
35
Multimodal imaging of a 35 year-old
woman with acute zonal occult outer
retinopathy (AZOOR). Color fundus
photography (Color) revealed subtle
peripapillary pigmentary abnormalities.
Fundus autofluorescence (FAF) showed a
sharply demarcated area of
hypoautofluorescence with a
hyperautofluorescent border. Optical
coherence tomography (OCT) showed
disruption of the outer retinal structures,
including the ellipsoid zone and
photoreceptor outer segments (arrow), in
the area of FAF abnormalities.

36. Points regarding AZOOR to remember
• F>M, 3 and 4 th decade, myope , viral prodrome usually +
• Bilateral but starts in one eye initially, DV, photopsias, field defect
moving colors in the field defect area
• AC quiet, few vitreous cells+, fundus initially may appear normal,
pigmentary changes occur peripapillary zone. May resemble RP in
later stages
• VF defects temporal and then spread centrally
• OCT shows loss of EZ and outer photoreceptors , later-outer and
inner nuclear layer atrophy later
• ERG always abnormal and shows reduced amplitudes
• In 1/3 recurs but most patients maintain VA 20/40, field defects
stabilize and in some it improves
• No known treatment but steroids and immunosuppressives have
been tried in recurrent and chronic cases
36

37. Acute Macular Neuroretinopathy
• Usually young females, males very rare
• Patients present with acute onset of visual field defects near the center or
decreased vision. VA usually 20/40 in most cases
• Unilateral or bilateral
• Fundoscopy usually shows bilateral parafoveal wedge shaped reddish
brown or orange color lesion or petalloid, teardrop, or horseshoe shaped
lesion
• Visual field testing shows corresponding paracentral scotomas
• Retinal vessels and ONH are not affected
• No vitritis no AC activity
• The AMN lesions resolve over several weeks with recovery of visual fields
• Recent viral illness, oral contraceptive use, exposure to sympathomimetics
may be present
• The lobular shape of retinal lesions suggest involvement of choriocapillaris
lobules
37

38. Investigations
• Near Infrared reflectance imaging- shows typical wedge
shaped lesions near fovea
• FFA is usually normal
• SD OCT shows hyperreflectivity in outer plexiform,
outer nuclear layers and disruption of ellipsoid zone,
outer segment, interdigitation zones
• OCT angio has shown defects in choriocapillaris plexus
and some cases in deep retinal capillary plexus
• Later OCT show thinning of outer nuclear layer and
outer plexiform layer
38

39. Treatment
• Usually no treatment is needed as most cases
resolve with time and field defects slowly
disappear
• Prognosis is good
39

40. Munk et al Br J Ophthalmol 2017;101(2):16-165
40

41. Munk et al Br J Ophthalmol 2017;101(2):16-165
41

42. Acute Macular Neuroretinopathy-
summary
• Young female patients, bilateral or unilateral
• Sudden onset of field defects in the central field with
corresponding wedge shaped or petalloid shaped orange
colored lesions at outer retina better seen on Near infrared
reflectance (NIR) imaging
• No AC activity, no vitreous cells, no disc swelling, FFA
normal
• OCT shows hyperreflectivity at outer plexiform and outer
nuclear layers and attenuated reflectivity from ELM, EZ and
interdigitation zone
• OCT angio shows disturbed circulation in choriocapillaris
lobes under the lesions
• Most heal without treatment with good visual recovery
42

43. Birdshot Retinochoroidopathy (BRC)
Fig from Quillen et al AJO 2004
43

44. Birdshot retinochoroidopathy BRC
• Bilateral disease
• Age 40-60 years, F>M
• Pt c/o DV out of proportion to the VA, floaters, photopsias and later stages
night vision and color vision difficulties
• Early stages the fundus lesions may be less prominent leading to missing
the diagnosis (AZOOR ALSO MAY MISS DIAGNOSIS)
• Anterior segment reaction absent Vitritis always present
• Orange yellow lesions with indistinct borders are present at deep retina
and radiate from ONH - typical lesions resemble bird shots
• They are ¼ to ½ DD is size
• Lesions are mainly nasal and inferior retina and radiate to periphery
• Usually symmetric in both eyes
• Retinal vasculitis is present and is seen mostly as narrowing of vessels
• Recurrent and chronic course leads to CME, foveal atrophy, ONH pallor like
in glaucoma
44

45. Investigations
FFA-
• Circulation time delayed but vessels empty the dye early-quenching
• Leakage from vasculitis affected vessels, ONH leakage and CME
leakage
• The lesions may not be shown if active if they are atrophic the RPE
window defect may be seen
ICG-shows the lesions to be hypocyanant in early and late phases and
aligned along the choroidal veins
ERG- decreased scotopic b wave amplitude, 30hz flicker implicit time
abnormal
• Visual field – peripheral field constriction, enlarged blind spot and
scotomas
• OCT shows- atrophy of Sattler layer in choroid on EDI
• HLA-A29+VE nearly 100%
45

46. Treatment
• Oral Cyclosporine or Azathioprine or
Mycofenolate mofetil
• Systemic steroids lower dose
• Infliximab has been shown to be effective
• Intravitreal steroids for CME
• CNV-treat by anti VEGF
• Long term prognosis for vision is guarded as
CME, CNV, ONH atrophy affect the vessels
46

47. BRC summary
• 40-60 years old F>M, bilateral
• DV out of proportion to the VA, photopsias, field
defect, difficulties in dark vision and color
• AC clear, vitritis+, ONH hyperemia later pallor,
yellowish orange lesions mainly nasally and inferiorly
radiating from disc to the equator, ¼ to ½ DD large with
faint borders, vessel narrowing CME, ONH pallor
• ICG shows all lesions as hypocyanascent, FFA shows
dye quenching -early emptying of vessels , HLA-A29+ve
in 90%, ERG always abnormal
• Chronic with poor prognosis
47

48. Knickelbein et J Clin Exp Ophthalmol
.2016;7(3): 570
48

49. Knickelbein et J Clin Exp Ophthalmol .2016;7(3): 570
Multimodal imaging of a 53 year-old woman with birdshot chorioretinopathy (BCR). On presentation, the hypopigmented birdshot
lesions seen on color fundus photography (Color) appear as hypofluorescent spots on late indocyanine green angiography (Late
ICGA). 6 months later, after receiving treatment with oral prednisone and mycophenolate mofetil, the lesions are essentially
unchanged on color photographs, while late ICGA reveals substantially fewer dark spots.
49

50. Serpigenous choroidopathy
• A rare condition that affects M>F, 2-7th decade
• Bilateral but asymmetric, progressive and chronic affecting the RPE and choroid
• Recurrences occur weeks to months later after initial episode
• Pts present with c/o in one eye of DV, photopsias, metamorphopsias, scotomas,
visual field defects
• Anterior segment normal, vitritis mild+, acute lesions start near ONH or macula &
have whitish/creamy color, jig saw puzzle shape with ill defined borders at RPE and
choriocapillaris level
• Subretinal fluid may be present over the lesions
• The acute lesions resolve over 8 weeks extensive RPE atrophy and
hyperpigmentation and new lesions start near the border of the old lesions and
spread outward in snake like fashion –so serpigenous or helicoid
• Multiple stages of lesions can be seen in the same eye- fresh lesions, healing
lesions, RPE atrophy with hyper pigmented areas
• If macula is involved then the vision may be affected permanently as also the risk
of CNV increases –occurs in 25% patients
• HLA B7 higher % seen and high retinal antigen s seen
50

51. 51
RAVEN ET AL

52. 52
Quillen et al AJO 2004

53. Investigations
• FFA- active lesions show hypofluorescence over the lesions with
hypefluorescence over the active edge of the lesions
• ICGA shows four stages-Hypocyanescent in subclinical choroidal
stage 1()and active stages (2), hypercyanescent in healing stage )
and hypocyanescent in the atrophic or scar stage
• OCT shows hyperreflectivity and thickening of retina over active
lesions with EZ disturbed. Choroid also shows hyperreflectivity in
old lesions due to RPE atrophy water fall effect
• Important to keep in mind that TB causes a serpigenous like
chorioretinopathy(SLC) and hence ruling out TB is very important
• Etiology is supposed to be immune mediated
53

54. Treatment
• Usually frustrating
• The treatment should be started in acute phase
• Oral steroids are not that efffective
• Immunomodulators like azathioprine, cyclosporine and
methotrexate have been tried with varying success
• CNV can be treated by intravitreal anti VEGF injections
• Visual prognosis is guarded and macular atrophy and
subfoveal CNV affect the vision severely
•
54

55. 55
Brydak-Godowska et al Medical Science monitor 2017;23:1106-1115
Active
edge

56. Knickelbein et J Clin Exp Ophthalmol .2016;7(3): 570
• Multimodal imaging of a 67 year-old man
with serpiginous choroiditis. During a period
of quiescence, color fundus photography
demonstrates a helicoid pattern of
chorioretinal atrophy emanating from the
optic nerve (Baseline Color), while fundus
autofluorescence shows corresponding areas
of hypoautofluorescence (Baseline FAF). 5
months later, despite immunosuppressive
therapy, disease activity returned with a new
area of retinal whitening on color fundus
photography (5 months Color, arrow). The
newly active lesion appeared mostly
hyperautofluorescent on FAF. Optical
coherence tomography demonstrated outer
retinal loss and RPE disruption in the areas of
lesions. An infrared reflectance (IR) image is
shown to demark the location of OCT B
scans.
56

57. Serpigenous Choroiditis Summary
• Bilateral but asymmetric, M>F, 2nd to 7th decades, chronic
recurrent disease, present with DV, photopsia,
metamorphopsia, scotomas, HLA B7 may be positive
• Vitritis mild, greyish white lesions start near ONH or macula
and spread in helicoid fashion. Old lesions heal over 8
weeks with RPE atrophy and hyperpigmentation
• Recurrences occur at the edge of healed lesions
• VA affected by macular atrophy or by CNV
• FFA shows hypo fl over the active lesion and hyperfl at the
edge old lesions show RPE window defect
• Treatment is aggressive immunosuppressive treatment
from the beginning and long treatment
• Prognosis is not good
57

58. Punctate Inner choroidopathy (PIC)
• Young, female myopic patients, caucasians
• Present with DV, photopsias, paracentral scotomas and
metamorphopsias
• No anterior uveitis or vitritis
• Fundus shows well delineated 100-300 mu yellowish white
lesions over the posterior pole at the level of RPE,
CHOROID & outer retina
• These lesions may coalesce and serous RD over the lesions
may be present
• Over time they heal by developing well punched out yellow
white atrophic scars which later may become pigmented
• CNV can develop in acute stage in about 40%
58

59. 59

60. Investigations
• OCT- focal elevation of RPE with thinning of outer
retinal layers and choroid
• FFA-Active lesions are hyperfluorescent with
staining in late phase. Show more lesions than
seen ophthalmoscopically. Atrophic lesions will
show RPE window defect. CNV will show
hyperfluorescence with leakagge
• ICG-hypocyanant lesions
• FAF- hypo autofluorescent lesions with hyper
autofl borders
60

61. Brydak-Godowska et al Medical Science monitor 2017;23:1106-1115
61

62. Treatment & prognosis
• Treat the complication of CME and CNV which
affect vision
• CNV is treated by anti VEGF
• Recurrence are common so need careful
observation
62

63. PIC
• PIC sometimes develops more lesions and
scars and may evolve in to Multifocal
choroiditis with panuveitis or sometimes
subretinal fibrosis
63

64. PIC summary
• Young female myopes affected
• Bilateral, AC quiet, no Vitritis
• Yellowish white well marked lesions over the posterior pole
with sometimes serous retinal detachment over lesions in
acute stage
• Later lesions develop well demarcated atrophic scars with
some pigmentation
• Patients can develop CNV in acute stage or late in 40-75%
patients
• Treat CNV or CME
• CNV by anti VEGF
• Prognosis is guarded as recurrent CNV can occur
64

65. 65
FROM QUILLEN ET AL AJO 2004

66. 66
FROM QUILLEN ET AL AJO 2004

67. 67
Crawford et al ISRN Inflammation 2013, Article ID 783190

68. 68
Crawford et al ISRN Inflammation 2013, Article ID 783190