HOW 3D OCT ENHANCESAMD & DME TREATMENT

The Retina Centers Of Washington

Georgetown University

Rockville- Arlington offices

T.S. Melki, MDJan 15, 2012

Anatomy of the Retina

Age-Related Macular Degeneration (AMD) Defined

AMD= disease associated with aging that gradually destroy sharp, central vision.

AMD can advance so slowly that people notice little change in their vision. In others, it can progresses much faster and may lead to a loss of vision in both eyes.

Two types: Dry and Wet AMD

Dry AMD Occurs when the light-sensitive cells in the

macular slowly breakdown, cause gradually blurring central vision.

Three stages of dry AMD:1- Early AMD: several small or medium-sized

drusen. Patients have no symptoms.2- Intermediate AMD: many medium-sized or one

or more large drusen. They can see a blurred spot in the center of their vision.

3- Advanced Dry AMD: in addition to drusen, patients have a breakdown of light sensitive cells, causing blurred spot in the center and getting bigger over time.

Wet AMD Wet MD occurs when abnormal blood

vessels behind the retina start to grow under the macular.

These new blood vessels tend to be very fragile and often leak blood and fluid.

The blood and fluid raise the macular from its normal place, causing macular edema.

Loss of central vision occur quickly without treatment.

Wet AMD

Epidemiology

The Beaver Dam Eye Study: 30% individuals aged >75 have some

form of AMD 7% of those have an advanced form

Recent studies:

8 million Americans to be at risk of developing advanced AMD in the next 5 years

Epidemiology

The cause of AMD remains unknown Mild association between hypertension and

AMD Smoking has been demonstrated to be the

most consistence modifiable risk factors Greater levels of plasma vascular endothelial

growth factor (VEGF), von Willebrand factor, and fibrinogen, as well as increased plasma viscosity, in patients with AMD

Treatment for Dry AMD

Once dry AMD reaches the advanced stage, no treatment can prevent the vision loss.

However, treatment can delay and possibly prevent intermediate AMD from progressing to the advanced stage.

The National Eye Institute’s Age-Related Eye Disease Study (AREDS) : taking a specific high-dose formulation of antioxidants and zinc reduces the risk of advanced AMD.

Treatment for Wet AMD 1. Laser surgery: Using laser to destroy the

fragile, leaky blood vessels. However, laser treatment may also destroy some surrounding healthy tissue and some vision.

2. Photodynamic therapy: using drug called verteporfin inject intravenous. The drug tends to stick to the surface of the new blood vessels, then a light is shined into the eye to activate the drug destroy the new blood vessels.

Treatment for Wet AMD ( cont.)

3. Injections Using anti-VEGF drugs ( Avastin,

Lucentis …) to inject into the vitreous. These drugs act on blocking the effects of the growth factor which present with high level in AMD and promote the growth of abnormal new blood vessels

Intra-vitreal injection Avastin or Kenalog

Avastin- Mechanic of Action

Treatment for WET AMD (cont.)

T.T.T. (TRANS-PUPILLARY-THERMAL-THERAPY)

-USING THE DOIDE LASER TO HEAT

AND COAGULATE THE CHOROIDAL

ABNORMAL VESSELS, WITH MINIMAL

DAMAGE TO THE NORMAL RETINAL

TISSUE.

ANTI VEGF-VEGF has been show to be an endothelial cell-specific mitogen and an angiogenic inducer, also known as a vascular permeability factor.

-Hypoxia has been shown to be a major inducer of VEGF gene transcription.-All variants of VEGF (particularly VEGF-A) have been implicated in the occurrence of increased vascular permeability by affecting endothelial tight-junction proteins in ocular vascular diseases.

-Levels of VEGF-A are considerably higher in AMD patients with extensive leakage in the macular region.

- Human VEFG is found in at least 9 isoforms.

-Currently anti VEFG drugs are:o Pegaptanib sodium (Macugen; OSI Eyetech Pharmaceuticals, Melville, NY)- Not available in the market any more.o Ranibizumab (Lucentis, Genentech Inc.,San Francisco, CA)o Bevacizumab (Avastin; Genentech Inc., San Francisco, CA)o Eylea ( Aflibercept; Regeneron )

-Avastin is a complete full-length humanized antibody that binds to all subtypes of VEFG and is used succesfully in tumor therapy as a systemic drug. (Colon CA.)

-Studies have demonstrated that intravitreal injection of Avastin haspromising effects in the reduction of ME secondary to CRVO , vascularpermeability, and fibrovascular proliferation in retinal neovascularizationsecondary to PDR , rubeosis iridis, ROP, CNV secondary to AMD, and in the treatment of DME.

Wet AMD case 1

Wet AMD case 1- s/p 1st IVA

Wet AMD case 1-recurrent

Wet AMD case 1-s/p 2nd IVA

AMD case 2

AMD case 2 (cont.)

AMD case 2 – s/p IVA

Case 3-Before IVL

Case 3: After IVL – 5 weeks

Case 3: 2 mos- slightly increasing fluid

Case 3: after reinjected IVA

Case 4: Before IVA

Case 4: After IVA – 6 weeks

Case 5

Case 5- Fluoresceine

Case 6- Before and after IVA

Case 7: Wet AMD, 2-mo s/p IVA

Newly defined: Age-related Choroidal Atrophy

Spaide RF report:

-Using Enhanced depth imaging spectral-domain optical

coherence tomography (EDI OCT).

-Age-related choroidal atrophy affects older individuals in

whom posterior pole abnormalities develop that may

mimic and also be associated with findings typical for

AMD.

-Decreasing choroidal thickness could represent an

increasing risk of retinal degeneration.

Diabetic Retinopathy - Epidemiology

18 million adults in United States

30% undiagnosed

WHO: 4% 1995 to 5.4% in 2025

Developed countries: 6.0% to 7.6%

24,000 become legally blind each year

DR leading cause of legal blindness in adults: 8% of cases

Over age 50: visual impairment 23.5% diabetics

Increased risk of glaucoma and cataracts

Epidemiology ( cont.)

Diabetic retinopathy affects 50%

More than 5 million have DR

700,000 cases PDR annually

26% with DM for 25-50 years develop PDR

Type I greater risk than Type II

DIABETIC MACULAR EDEMA

NPDR

The International Clinical Diabetic Macular Edema Disease Severity Scale includes two major levels:

1. Absent of DME2. Present of DME :

Mild (some retinal thickening or hard exudates in the posterior pole, but distant from the center of the macula).

Moderate(retinal thickening or hard exudates approaching the center of the macula but not the center).

Severe(involving retina thickening or hard exudates involving the center).

DME

POST AVASTIN

DME

POST SUBTENON KENELOG

Diabetic macular edema

After STK treatment – 6 weeks

Diabetes, s/p Subtenon 8 Weeks

Thank you for your attention

Questions are welcome