OCT Ango in ARMD and telangictasia.pptx

1. OCT Angio in ARMD
Nagla Hassan MD
MIOR-Egypt

2. ARMD
ARMD is thought to be a group of genetically,
environmentally-determined retinal degenerative , age related
diseases, of the RPE cells ,which are essential for photoreceptor
metabolism and removal of waste products. Dysfunctional cells
accumulate undigested waste, which is clinically evident as focal
yellow subretinal clumps, termed drusen.
Drusen are the herald of ARMD, and large or numerous
drusen are poor prognostic factors for future visual loss. The
disruption of photoreceptor metabolism eventually causes areas of
retinal atrophy or neovascularization.

4. Risk factors forAMD
4
 Age1
-Genetic factors
-Smoking
-Hypertension and cardiovascular
disease
-Race
-High cholesterol
-Low intake of antioxidants

11. Dry type ARMD
Areas of impaired choriocapillaris flow typically extended
beyond the borders of the geographic atrophy GA.
Eyes with dry AMD were shown to have a generalized
decrease in choriocapillaris density, which was sometimes
associated with drusen

13. The soft drusen shown are associated with areas of
decreased signal in the choriocapillaris, which could
indicate flow impairment

14. Soft drusen demonstrating an area of decreased signal
in the choriocapillaris underlying the drusen.

16. OCTA in Neovascular AMD
Calcifications:
Type 1 40% under the RPE
Type 2 9 % subretinal
Type 3 34% intraretinal (RAP)
Type 4 17% mixed

17. Choriocapillaris and the outer retina are
shown two nets of abnormal vessels are
shown surrounded by relatively
homogenous choriocapillaris.
The abnormal vessels exist both below and
above Bruch’s membrane.
Sulzbacher F, Pollreisz et al.

18.  Abnormal vessels are shown surrounded by
relatively homogenous choriocapillaris
Kuehlewein L, Bansal M, et al.

19. OCT angiogram segmented so the choriocapillaris are shown. A
circular net of abnormal vessels are shown surrounded by
relatively homogenous choriocapillaris.The abnormal vessels exist
both below and above Bruch’s membrane (in the outer retina).

20. LUMBROSO B, RISPOLI M ET AL

28. OCTA showed a membrane was identified as sea fan

29. OCTA showed a membarne idinfied as medussa

30. OCTA shaowed membranes lacking such distinct
membrane morphology-ill-defined

31. The membrane was identified as long filamentous if
the membrane had a dead-tree

34.  Sulzbacher F, Pollreisz et al.

35.  Sarks SH. Br J Ophthalmol.

36. Role of VEGF-Ain wetAMD progression
VEGF-A
Migrating
endothelial cells
form new blood
vessels in formerly
avascular space
Hypoxia
Proliferation
Migration
Proteolysis
Vascular
endothelial cell
Other angiogenic
growth factors
Basement
membrane

37. VEGF inhibitors
Anti-VEGF therapies are
established as a key
molecule in neovascular
AMD therapies
37

39. Before and after treatment

40. Before and after injection

42. Dead tree

43. DEAD TREE

44. PED without any neovessles
Huang D, Swanson EA, Lin CP, Schuman JS, Stinson WG, et al.

46. Stages
Stage I: Intraretinal Neovascularization (IRN)
Vascular proliferation originates from the deep capillary plexus of the retina in the
paramacular area and is confined within the retina, as a retinal-retinal
anastomosis. Intraretinal haemorrhage and edema are common.
Stage II: Subretinal Neovascularization (SRN)
Neovascularization invades sub retinal space (above/superficial to the retinal
pigment epithelium). Neurosensory and serous pigment epithelial detachment can
be found, together with increasing edema of the retina and haemorrhages in the
pre-retinal and intraretinal spaces.
Stage III: Choroidal Neovascularization (CNV)
Choroidal neovascularization (subretinal pigment epithelium) is present. It can be
associated with vascularized pigment epithelial detachment. A retinal-choroidal
anastomosis is formed.

48. Shows a large anomalous vessel in the deep retinal plexus The
hyper-reflective foci observed on structural SD-OCT (middle)
within this particular location have abnormal flow

49. OCTA en face images show the RAP lesion in the
superficial, deep, and avascular segments of
the retina, respectively

50. Type 3 RAP
High flow transverses the inner and outer retina and
extends below the RPE which corresponding to
hyperreflective lesion in the B scan

52. RAP with no extension to sub RPE before and after
injection

53. Myopic CNVM

55. Retinal Telangiectasia

57. Stage 2 macular Telangiectasia with dilated feeder
and draining vessels

59. Stage 2 macular Telangiectasia with dilated feeder and draining vessels

60. Chronic CSR
CNVM

61. The disease may be complicated by type 1 (CNV) However
,this complication may be difficult to diagnose because
chronic CSC and type 1 CNV share many signs on both FA
and OCT and
CNVM is more common in certain eyes with chronic CSCR
Old age undergone
laser photocoagulation
Diffuse RPE
irregularities
&undulating RPED
Hindawi -Journal of Ophthalmology 2018.
Intraretinal fluid or
diffuse SRF

62. Types of CNVM in Chronic SCCR by OCTA
Sea Fan
Poorly
circumscribed