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.
EpidemiologyThe Beaver Dam Eye Study: 30% individuals aged >75 have some form of AMD 7% of those have an advanced formRecent 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
Treatment for WET AMD (cont.)T.T.T. (TRANS-PUPILLARY- THERMAL-THERAPY)-USING THE DOIDE LASER TO HEATAND COAGULATE THE CHOROIDALABNORMAL VESSELS, WITH MINIMALDAMAGE TO THE NORMAL RETINALTISSUE.
ANTI VEGF-VEGF has been show to be an endothelial cell-specificmitogen and an angiogenic inducer, also known as avascular permeability factor.-Hypoxia has been shown to be a major inducer of VEGFgene transcription.-All variants of VEGF (particularly VEGF-A) have beenimplicated in the occurrence of increased vascularpermeability by affecting endothelial tight-junction proteinsin ocular vascular diseases.-Levels of VEGF-A are considerably higher in AMD patientswith 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)oEylea ( 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 inthe treatment of DME.
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.
18 million adults in United States30% undiagnosedWHO: 4% 1995 to 5.4% in 2025Developed countries: 6.0% to 7.6%24,000 become legally blind each yearDR leading cause of legal blindness in adults: 8% of casesOver age 50: visual impairment 23.5% diabeticsIncreased risk of glaucoma and cataracts
Diabeticretinopathy affects 50%More than 5 million have DR700,000 cases PDR annually26% with DM for 25-50 years develop PDRType I greater risk than Type II
The International Clinical Diabetic Macular EdemaDisease Severity Scale includes two major levels: 1. Absent of DME 2. 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).