January 16, 2019

H.Razmjuo MD

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

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

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

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

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

Macular edema Focal Diffuse

CSME Eyes with CSME benefited from focal argon laser photocoagulation .

Laser The mainstay of treatment for PDR involves the use of thermal laser photocoagulation in panretinal pattern to induce regression. 1200 or more 500-um burns. Treatment may be divided in to 2 or more sessions.

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

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

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.

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

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.

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.

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.

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.

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

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

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.

Patient 1 Pre-Evastin

Patient 1 Post-Evastin 5 days later

patient2 Pre-Evastin

Patient 2 Post-Evastin 2 weeks later

Patient 3 Pre-evastin

Patient 3 Post-Evastin 16 days later

Patient 4 Pre-evastin

Patient 4 Post-Evastin 16 days later

Thanks for your attention