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DIABETIC
RETINOPATHY
SOUMIK SEN
MB140039
PROLIFERATIVE DIABETIC
RETINOPATHY
 Proliferative diabetic retinopathy affects 5-10% of the
diabetic population.
 Type 1 diabetics are particularly at risk with an
incidence of about 60% after 30 years of onset of
diabetes.
 Therefore it is more common in patients with juvenile
onset diabetes.
PATHOGENESIS
 Occurrence of neovascularization is the hallmark of PDR.
It occurs over the changes of NPDR.
 Caused by angiogenic growth factors elaborated by
hypoxic retinal tissue in an attempt to revascularize
hypoxic retina.
 These substances promote neovascularization on the
retina and the optic head and occasionally on the iris.
 VEGF, placental growth factor and pigment epithelium
derived factor appears to be of particular importance.
 It usually occurs along the course of major temporal
retinal vessels.
DIAGNOSIS
 NEOVASCULARIZATION AT DISC: Describes neovascularization on or
within one disc diameter of the optic nerve head.
 NEOVASCULARIZATION ELSEWHERE: Describes neovascularization
along the course of the major vessels.
 FLUORESCENT ANGIOGRAPHY: Highlights the neovascularization
during the early phases and shows hyper fluorescence due to
leakage of dye from neovascular tissue.
NEOVASCULARISATION AT THE
DISC (NVD)
NVD
NEOVASULARISATION
ELSEWHERE (NVE)
NEOVASCULARISATION AT THE
IRIS (NVI)
NEOVASCULARISATION AT THE IRIS
NEOVASCULAR GLAUCOMA
VITREOUS CHANGES
VITREOUS HAEMORRHAGE TRACTIONAL RETINAL DETACHMENT
FURTHER CLASSIFICATION
OF PDR
 On the basis of high risk characteristics(HRCs) described by
the diabetic retinopathy study(DRS) group, PDR can be
further classified into:
1. EARLY NVD OR NVE PDR without HRCs (EARLY PDR).
2. PDR with HRCs.
HIGH RISK
CHARACTERISTICS
 NVD 1/4TH TO 1/3RD of disc area with or without vitreous
hemorrhage or pre-retinal hemorrhage.
 NVD <1/4TH disc area with vitreous hemorrhage or pre-
retinal hemorrhage.
 NVE >1/2 disc area with vitreous hemorrhage or pre-retinal
hemorrhage.
DIABETIC MACULOPATHY
 Most common cause of visual impairment in diabetic patients,
particularly type 2.
 Diffuse retinal edema is caused by extensive capillary leakage and
localized edema is caused by focal leakage from microaneurysms
and dilated capillary segments.
 The fluid is initially located between outer plexiform and inner
nuclear layers; later it may also involve the inner plexiform and the
nerve fibre layers, until eventually the entire thickness of the retina
becomes edematous.
WHY IS DIABETIC MACULAR
EDEMA SO IMPORTANT?
 The macula is responsible for central vision.
 Diabetic macular edema may be
asymptomatic at first. As the edema moves
in to the fovea (the center of the macula) the
patient will notice blurry central vision. The
ability to read and recognize faces will be
compromised.
CLINICO-ANGIOGRAPHIC
CLASSIFICATION OF DIABETIC
MACULOPATHY1. FOCAL EXUDATIVE MACULOPATHY
2. DIFFUSE EXUDATIVE MACULOPATHY
3. ISCHAEMIC MACULOPATHY
4. MIXED MACULOPATHY
FOCAL EXUDATIVE
MACULOPATHY SIGNS: Micro aneurysm, hemorrhages and well circumscribed macular
edema and hard exudates arranged in a circinate pattern.
 FA: Focal area or hyperfluorescence due to leakage and good macular
perfusion.
DIFFUSE EXUDATIVE
MACULOPATHY SIGNS: Diffuse retinal edema and thickening throughout the posterior pole
with relatively few hard exudates.
 FA: Extensive hyper fluorescence at the posterior pole due to leakage.
ISCHAEMIC MACULOPATHY
 It occurs due to microvascular blockage.
 SIGNS: micro aneurysms, dot and blot hemorrhage, mild or no macular
edema and few hard exudates.
 FA: capillary non perfusion at the fovea and frequently other areas of
capillary non-perfusion at the posterior pole and periphery.
CLINICALLY SIGNIFICANT
MACULAR EDEMA
 It is diagnosed if one of the following three criteria are present
on slit lamp examination with 90D lens.
1. Thickening of the retina at or within 500 µm of the center of
the fovea.
2.Hard exudates at or within 500 µm of the center of the fovea, if
associated with thickening of the adjacent retina.
3.Area of retinal thickening 1 disc diameter or larger in size,
within 1 disc diameter of the center of the fovea.
CSME
Retinal oedema
within 500 microns of
centre fovea
Hard exudates within
500 microns of fovea if
ass with adjacent retinal
thickening
Retinal oedema > 1 disc
diameter, any part is
within 1 disc diameter of
centre of fovea
ADVANCED DIABETIC EYE
DISEASE Serious vision-threatening complications of DR.
 Occurs in pts who have not had laser therapy or in whom laser
photocoagulation has been unsuccessful.
 Complication:
1. Persistent vitreous hemorrhage
2. Tractional retinal detachment
3. Opaque membrane formation
4. Neovascular glaucoma
 Treatment: Pars plana vitrectomy.
 Poor prognosis
MICROANEURYSMS
DOT AND BLOT
HEMORRHAGE
HARD EXUDATES
COTTON WOOL SPOTS
VENOUS BEADING
IRMA

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Diabetic Retinopathy- PDR and CSME

  • 2. PROLIFERATIVE DIABETIC RETINOPATHY  Proliferative diabetic retinopathy affects 5-10% of the diabetic population.  Type 1 diabetics are particularly at risk with an incidence of about 60% after 30 years of onset of diabetes.  Therefore it is more common in patients with juvenile onset diabetes.
  • 3. PATHOGENESIS  Occurrence of neovascularization is the hallmark of PDR. It occurs over the changes of NPDR.  Caused by angiogenic growth factors elaborated by hypoxic retinal tissue in an attempt to revascularize hypoxic retina.  These substances promote neovascularization on the retina and the optic head and occasionally on the iris.  VEGF, placental growth factor and pigment epithelium derived factor appears to be of particular importance.  It usually occurs along the course of major temporal retinal vessels.
  • 4. DIAGNOSIS  NEOVASCULARIZATION AT DISC: Describes neovascularization on or within one disc diameter of the optic nerve head.  NEOVASCULARIZATION ELSEWHERE: Describes neovascularization along the course of the major vessels.  FLUORESCENT ANGIOGRAPHY: Highlights the neovascularization during the early phases and shows hyper fluorescence due to leakage of dye from neovascular tissue.
  • 6. NVD
  • 8. NEOVASCULARISATION AT THE IRIS (NVI) NEOVASCULARISATION AT THE IRIS NEOVASCULAR GLAUCOMA
  • 9. VITREOUS CHANGES VITREOUS HAEMORRHAGE TRACTIONAL RETINAL DETACHMENT
  • 10. FURTHER CLASSIFICATION OF PDR  On the basis of high risk characteristics(HRCs) described by the diabetic retinopathy study(DRS) group, PDR can be further classified into: 1. EARLY NVD OR NVE PDR without HRCs (EARLY PDR). 2. PDR with HRCs.
  • 11. HIGH RISK CHARACTERISTICS  NVD 1/4TH TO 1/3RD of disc area with or without vitreous hemorrhage or pre-retinal hemorrhage.  NVD <1/4TH disc area with vitreous hemorrhage or pre- retinal hemorrhage.  NVE >1/2 disc area with vitreous hemorrhage or pre-retinal hemorrhage.
  • 12. DIABETIC MACULOPATHY  Most common cause of visual impairment in diabetic patients, particularly type 2.  Diffuse retinal edema is caused by extensive capillary leakage and localized edema is caused by focal leakage from microaneurysms and dilated capillary segments.  The fluid is initially located between outer plexiform and inner nuclear layers; later it may also involve the inner plexiform and the nerve fibre layers, until eventually the entire thickness of the retina becomes edematous.
  • 13. WHY IS DIABETIC MACULAR EDEMA SO IMPORTANT?  The macula is responsible for central vision.  Diabetic macular edema may be asymptomatic at first. As the edema moves in to the fovea (the center of the macula) the patient will notice blurry central vision. The ability to read and recognize faces will be compromised.
  • 14. CLINICO-ANGIOGRAPHIC CLASSIFICATION OF DIABETIC MACULOPATHY1. FOCAL EXUDATIVE MACULOPATHY 2. DIFFUSE EXUDATIVE MACULOPATHY 3. ISCHAEMIC MACULOPATHY 4. MIXED MACULOPATHY
  • 15. FOCAL EXUDATIVE MACULOPATHY SIGNS: Micro aneurysm, hemorrhages and well circumscribed macular edema and hard exudates arranged in a circinate pattern.  FA: Focal area or hyperfluorescence due to leakage and good macular perfusion.
  • 16. DIFFUSE EXUDATIVE MACULOPATHY SIGNS: Diffuse retinal edema and thickening throughout the posterior pole with relatively few hard exudates.  FA: Extensive hyper fluorescence at the posterior pole due to leakage.
  • 17. ISCHAEMIC MACULOPATHY  It occurs due to microvascular blockage.  SIGNS: micro aneurysms, dot and blot hemorrhage, mild or no macular edema and few hard exudates.  FA: capillary non perfusion at the fovea and frequently other areas of capillary non-perfusion at the posterior pole and periphery.
  • 18. CLINICALLY SIGNIFICANT MACULAR EDEMA  It is diagnosed if one of the following three criteria are present on slit lamp examination with 90D lens. 1. Thickening of the retina at or within 500 µm of the center of the fovea. 2.Hard exudates at or within 500 µm of the center of the fovea, if associated with thickening of the adjacent retina. 3.Area of retinal thickening 1 disc diameter or larger in size, within 1 disc diameter of the center of the fovea.
  • 19. CSME Retinal oedema within 500 microns of centre fovea Hard exudates within 500 microns of fovea if ass with adjacent retinal thickening Retinal oedema > 1 disc diameter, any part is within 1 disc diameter of centre of fovea
  • 20. ADVANCED DIABETIC EYE DISEASE Serious vision-threatening complications of DR.  Occurs in pts who have not had laser therapy or in whom laser photocoagulation has been unsuccessful.  Complication: 1. Persistent vitreous hemorrhage 2. Tractional retinal detachment 3. Opaque membrane formation 4. Neovascular glaucoma  Treatment: Pars plana vitrectomy.  Poor prognosis
  • 26. IRMA

Notes de l'éditeur

  1. Focal. (a) A ring of hard exudates temporal to the macula; (b) FA late phase shows focal area of hyperfluorescence due to leakage corresponding to the centre of the exudate ring.
  2. 2. Diffuse. (c) Dot and blot haemorrhages; (d) FA late phase shows extensive hyperfluorescence at the posterior pole due to leakage
  3. 3.Ischaemic. (e) Dot and blot haemorrhages and cotton-wool" spots; (f) FA venous phase shows hypofluorescence due to capillary non-perfusion at the macula and elsewhere