1. January 16, 2019

2. H.Razmjuo MD

3. Diabets mellitus
Type 1= immune – mediated diabetes – insulin – dependent diabetes mellitus
Type 2 = non insuline – dependent

4. Causes of decreased vision
Macular edema ( capillary leakage)
Macular ischemia ( capillary occlusion)
Sequelae from ischemia – induced neovascularization.

5. Types
Non proliferative diabetic retinopathy = (NPDR) background diabetic retinopathy
a) mild
b) moderate
c) severe
d) very severe

6. 2) Proliferative diabetic retinopathy ( PDR)
a) Early
b) high risk or advanced

8. NPDR can affect visual function by:
Increased intraretinal vascular permeability resulting in macular edema
Variable degrees of intraretinal capillary closure resulting in macular ischemia

9. Macular edema
Focal
Diffuse

12. CSME
Eyes with CSME benefited from focal argon laser photocoagulation .

14. Laser
The mainstay of treatment for PDR involves the use of thermal laser photocoagulation in panretinal pattern to induce regression or more 500-um burns. Treatment may be divided in to 2 or more sessions.

15. Focal laser side effects
Paracentral scotoma
Transient increased edema= decreased vision
Choroidal revascularization
Subretinal fibrosis
Photo coagulation scar expansion
Inadvertent foveolar burns

19. PRP
1200 or more 500-um burns separated by one – half burn width. Surrounding ring of edema making many of the burns appear confluent

22. Drug therapy
Intravitreal drug therapy was first used over 30 years ago, when antibiotics were injected into the eye to treat vision threatening eye infections.
These injections were shown to be safe and effective. More recently, steroid, antiviral and antibodies (Avastin) which block abnormal blood vessel growth have been developed for intraocular use.

23. Medical management of DME
1)Long acting steroids(Triamcinolon 4mg) 2)Antiv ascular endothelial growth factor (AVEG 1.5 mg)

24. Medical manement of DME
1) Sub- Tenon injection of long acting steroid
In patients with refractory DME a posterior sub– Tenon injection of triamcinolone acetonide improved visual acuity at 1 month and stabilized vision up to 1 year in a retrospective interventional case series.
Arise in IOP was rare, as was ptosis.

25. 2)Intravitreal steroid
Similarly in patients with refractory CSME, intravitreal injection of corticosteroids was shown to modesty improve vision in the shout term and reduce macular thickness for up to 2 years of follow up. Post op cat and increased IOP were common but were manageable.

27. Anti VEGF
Vascular Endothelial Growth Factor (VEGF) is a substance which occurs naturally in the body. VEGF promotes blood vessel growth and makes retinal blood vessels leaky. Avastin is a drug which blocks VEGF, and was initially used systemically to stop new blood vessels from growing in patients with metastatic bowel cancer.

28. Avastin mechanism of action:
Patients with diabetic retinopathy have abnormally high levels of VEGF in their eyes. Blocking VEGF with Avastin can reduce vascular leakage and lessen macular edema.
Reducing macular edema can stabilize or improve vision.

29. Anti VEGF used for
Persistent macular edema unresponsive to retinal laser therapy
Rubeosis iridis
ROP
PDR
After cataract operation in patients with diabetic retinopathy
After deep vitrectomy operation in diabetic patients
In combination with ,laser and steroid]
Subfoveal neovascularization

30. Intravitreal bevacizumab 1
Intravitreal bevacizumab 1.5mg resulted in marked regression of neovascularization and rapid resolution of vitreous hemorrhage.

31. Complications
Injections to the eye are relatively safe. Hemorrhage, infection, cataract, and retinal detachment may occur, but are uncommon. Systemic risks include elevated blood pressure, stroke, and heart attack.

35. Patient 1
Pre-Evastin

36. Patient 1
Post-Evastin
5 days later

37. patient2
Pre-Evastin

38. Patient 2
Post-Evastin
2 weeks later

39. Patient 3
Pre-evastin

40. Patient 3
Post-Evastin
16 days later

41. Patient 4
Pre-evastin

42. Patient 4
Post-Evastin
16 days later

45. Thanks for your attention