PROLIFERATIVE

DIABETIC
RETINOPATHY
DR MAHNOOR
PGR-1
ASTEH
PATHOGENESIS
 Retinal ischemia due to widespread
capillary non perfusion results in the
production of VEGF(vascular
endothelial growth factors) and to the
development of neovascularization.
 Preretinal new vessels may arise
anywhere in the retina, they are
commonly seen at posterior pole.
 NVD describes neovascularization on
or within one disc diameter of optic
nerve head
 NVE describes
neovascularization
further away from
disc or elsewhere in
retina sometimes
along with fibrosis.
 NVI known as
rubeosis iridis
CLASSIFICATION
 Mild to moderate PDR:
new vessels on the disc (NVD) or new vessels elsewhere
(NVE),but extent insufficient to meet the high risk criteria
 High risk PDR:
NVD greater than ETDRS standard photo 10A (about 1/3
disc area)
Any NVD with vitreous hemorrhage
NVD greater than ½ disc area with vitreous hemorrhage
 Advanced diabetic eye disease
 HEAMORRHAGE
 Tractional retinal detachment:
posterior detachment in eyes with PDR is
incomplete
due to strong adhesions b/w cortical vitreous
and area of
fibrovascular proliferation.
 RUBEIOIS IRIDIS
NVI if severe may lead to neovascular
glaucoma
common in eyes with severe retinal ischemia
or persistent retinal detacment
HOW TO CHECK/EVALUATE
 FUNDUS CLINICAL
EVALUATION
 B SCAN (for vit hmg and RD)

 Fundus angiogram:
Highlights neovascularization and
leakage from tissue

FA can be used to confirm the

presence of new vessels if clinical
Diagnosis is in doubt
TREATMENT
 Disease counselling
 Intravitreal anti VEGF agents
 Intravitreal triamcinolone
 Scatter laser treatment(PRP)
 Pars plana vitrectomy
INTRA VITREAL INJECTIONS
 Pegaptanib (mucagen)
 Bevacizumab (avastin)
 Ranibizumab( lucentis)
 Aflibercept (eyelea)
 Sorafenib (Nexavar)
 Dasatinib (Sypracel)
 Sunitinib (Sutent)
 Pazopanib(Voteient)
VASCULAR ENDOTHELIUM
GROWTH FACTOR
 Hypoxia VEGF angiogenesis & neovascularization
 VEGF are of 7 types:

The significant is VEGF A increased vascular permeability &

angiogenesis
subtype variant of this is “ isomer VEGF -A165”

How the isomer works?

MECHANISM OF ANTI VEGF
 PEGAPTANIB (MACUGEN):
 Its RNA aptamer binds to VEGF A165
isomer
 0.3mg/0.05ml

 BEVACIZUMAB (AVASTIN):
 Full length recombinant humanized anti
VEGF monoclonal antibody
 148kDal
 1.25-2.5mg/0.05ml
 Ranibizumab (lucentis):
 Recombinant antibody fragment(only FAB moiety)
 0.3-0.5mg/0.05ml
 Aflibercept (eyelea):
 Recombinant fusion Protein of the binding domains of human VEGF-
R1 and R2 fused with Fc domain of IgG
 Traps the endogenous VEGF molecules
 Blocks VEGF-A VEGF-B ,Placental growth factor 1 &2
 PAN RETINAL
PHOTOCOAGULATION
 Panretinal photocoagulation
continues to be mainstay of
treatment for PDR
 DRS establishes the
characteristics of high risk
proliferative disease and
demonstrate the benefits of PRP
e.g NVD without hmg carries a
risk of visual loss BUT can
reduce due to PRP
VITRECTOMY
 INDICATIONS

 Severe persistent vitreous hemorrhage

 Progressive tractional RD
 Combined tractional and rhegmatogenous RD
 Premacular retrohyloid heamorrhage
 Anterior segment neovascularization and media opacity
BE GRATEFUL
EVERY
MOMENT..LIFE IS
UNPREDICTABLE
THANK YOU