how 3 d oct enhances amd & dme treatment
TRANSCRIPT
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