The macula is the most central portion of the retina, directly opposite the lens. It is where the greatest number of light sensitive cells, called cones, are located. Cones are the cells which allow us to see color and fine detail. The high concentration of cones in the macula gives people extremely detailed and rich central vision.
What is macular degeneration (AMD)?
AMD occurs when a layer under the retina is disrupted by deposits called drusen or other age-related changes. These changes may cause vision to deteriorate. When the macula breaks down, you lose your central vision, but it does not affect your peripheral (side) vision. There are two form of AMD, dry AMD, in which drusen causes aging and thinning of the macula. With dry AMD, vision loss is usually gradual. Wet AMD occurs when abnormal blood vessels develop under the retina. These vessels leak blood and fluid and blur central vision.
Central geographic atrophy, the “dry” form of advanced AMD, results from atrophy of the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. No medical or surgical treatment is available for this condition, however vitamin supplements with high doses of antioxidants, lutein and zeaxanthin, have been suggested by eye specialist to slow the progression of dry AMD and, in some patients, improve visual acuity.
Neovascular or exudative AMD, the “wet” form of advanced AMD, causes vision loss due to abnormal blood vessel growth (choroidal neovascularization) in the choriocapillaris, through Bruch’s membrane, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated.
Wet types of AMD have 10% of patients suffering from AMD.
Higher beta-carotene intake was associated with an increased risk of AMD.
What are the symptoms of AMD?
Signs and symptoms include:
Exudative changes: hemorrhages in the eye, hard exudates, subretinal /sub-RPE/ intraretinal fluid.
Atrophy: incipient and geographic.
Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80.
Preferential hyperacuity perimetry changes (for wet AMD).
Blurred vision: Those with nonexudative AMD may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative AMD often notice a rapid onset of vision loss.
Reduction or loss of central vision.
Distorted vision in the form of metamorphopsia, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at miniblinds in their home.
Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones.
Slow recovery of visual function after exposure to bright light.
A loss in contrast sensitivity.
How is AMD diagnosed?
Diagnostic include: ophthalmoscope examination, fluorescein angiogram (allows for the identification and localization of abnormal vascular processes), optical coherence tomography (used by most ophthalmologists in the diagnosis and the follow-up evaluation of the response to treatment by using either Avastin or Lucentis, which are injected into the vitreous humor of the eye at various intervals).
How is AMD treated?
Dry AMD – there is no treatment, though specific nutritional supplements may help slow its progression and impact.
Wet AMD – treatment options include thermal laser therapy, photodynamic therapy and anti-VEGF treatment. Anti-angiogenics or anti-VEGF agents can cause regression of the abnormal blood vessels and improve vision when injected directly into the vitreous humor of the eye. The injections must be repeated monthly or bimonthly.
The retina is a thin membrane which is held to the inside back portion of the eye by a kind of suction force. In the front part of the eye the retina is firmly attached at a ring just behind the lens called the pars plana. In the back part of the eye, the retina is continuous with the optic nerve which carries 3 million nerve fibers back to the brain. In between the pars plana and the optic nerve the retina is attached only by suction. The interior portion of the eye is filled with a material called vitreous, which is like a thin bag of jelly. As one gets older the vitreous tends to shrink, a process which is accelerated by prior cataract extraction or being greatly nearsighted. The bag of vitreous is also attached firmly in the front part of the eye at the pars plana. However, as the vitreous shrinks, it ultimately strips itself free from the surface of the retina in the back of the eye and begins to bobble around in the fluid. If it happens that the vitreous was glued on too tightly at a single point or several points just behind its firm attachment in the front part of the eye, the bobbling of the vitreous jelly bag can tear the retina at these points. Such a tear potentially breaks the suction holding the retina on. Depending upon the strength of the suction force that holds the retina on, the size of the tear, and the continued traction of the vitreous on the tip of the tear, the retina may detach.
Fixing Retinal Detachments
Retinal detachments are, in main, fixed by finding all of the tears and adequately closing them. It is both that simple and that complex.
The Bubble Procedure
Bubble procedure is, an injection of an expanding gas is made into the back of the eye with a short, very skinny needle. The patient is then asked to position themselves over the next 7-10 days in such a manner that the bubble, rising in the fluid in the back of the eye, plugs the tear(s). This reestablishes the suction, the fluid underneath the retina reabsorbs, and the retina reattaches. After that, the bubble is used like a splint. You can readily see that if the tear that needs to be closed is in the lower portion of the eye or if there are several tears widely spaced, this procedure cannot be effective and is therefore not offered. When the eye wakes up, the bubble is seen as a shimmering surface which is distinguishable from the retinal detachment by the fact that it is always seen as being on the floor no matter which way the head is moved. The bubble is reabsorbed by the blood stream and expelled through the lungs as a natural process over the next 7-10 days.
Advantages and Disadvantages
The bubble procedure has the advantage that it produces only minimal discomfort and the vision that will return tends to return quickly over a matter of days or weeks. It has two disadvantages: the need for positioning, which is mentioned above. Depending on the location of the tear, this can be anything from a minor nuisance to a major problem. Physical inability to maintain the position is one contraindication to doing this procedure. Secondly, if one takes all eyes to which the bubble is applicable, the procedure works only 7 or 8 out of 10 times. This does not mean that the other 2 or 3 out of 10 eyes go blind. It usually means that these eyes will later need scleral buckling, the other, more extensive procedure. Usually, the need for scleral buckling is obvious within the first few days.
The Scleral Buckle
The buckle begins, like the bubble, with anesthetic and freezing treatment. The tissues around the eye are then opened using scissors so that access can be gained to the side of the eyeball, on a spot or spots on the outside of the eye corresponding to where the tears are on the inside. A piece of silicone rubber is then sewn in such a way that when the sutures are tightened, the silicone indents the eye wall, making a hill on the inside of the eye for the tear to rest upon. Often, some of the fluid under the retina is drained out of the eye using a fine needle while the process is carefully monitored using the indirect ophthalmoscope. The drainage and the indentation from the buckle usually close the breaks.
Advantages and Disadvantages
This procedure has the advantage that it works 9 or 9.5 times out of 10 as a first procedure. The major advantage is that the ”buckle” typically does not require any special positioning. Furthermore, this procedure can be used to repair retinal detachments to which the bubble procedure cannot be usefully applied. It has the disadvantage that it typically hurts considerably more, at least for the following day or two, than does the bubble procedure. The vision that will return does so more slowly, typically over time measured in weeks or months, rather than days or weeks.
Once the retina is successfully reattached, the process of visual improvement begins. In the case where the center of the retina has not detached, the visual results are usually quite good. When the center of the retina has been detached, the visual results are less impressive, only rarely as good as the vision prior to the detachment, but sometimes close to it.
As stated above, the most common problem with each of these procedures is the possibility that the retina may not be attached in one operation. A subsequent attempt at repair can be entertained using a combination of these procedures or other available techniques not covered here (e.g., vitrectomy). About 7 in 100 eyes develop some generalized scarring referred to as PVR (proliferative vitreoretinopathy) which shortens the retina, makes it less elastic, and sometimes holds the breaks open despite efforts to close them. Usually, some combination of techniques can be used to repair retinas that develop this problem, but sometimes, even with the best efforts, PVR results in blindness. Other risks involved in these procedures include infection, perforation of the eye with the anesthetic needle, bleeding, double vision, glaucoma, and acceleration of cataract formation. All of these complications are quite uncommon.