MOVING into the zone

The ETDRS recommended treating up to 500 microns from the center of the fovea, but this is close, and you may want to play it safe and stay 750 microns from the center in order to avoid trouble. This is an easy number to define—just mentally split the diameter of the disc in half, and put one end at the center of the fovea. Until you have a lot of experience, or become cavalier (usually they are the same), it is best to avoid getting close to the center. This is where observant patients can really get frustrated, because they can detect your spots more easily. It is also where you can do some serious damage to the perifoveal capil lary network if you are not careful. A detailed angiogram is crucial before you work in this close, because you really need to be sure that you are not accidentally treating microaneurysms that happen to supply the few remaining capillaries that supply the fovea. If you shut them down, you can knock off large chunks of central vision, which is A Bad Thing.

Figure 10. This is why it is good to have an FA before treating near the fovea. The circle represents an estimate of 500 microns from the fovea based on the patient's nerve. The microaneurysms temporal to the fovea (between the arrows) are far enough away to be treatable if you decide to follow ETDRS guidelines. However, you can see from the FA that aggressive treatment of these little devils could shut down the only vessels supplying the entire temporal side of the fovea—you could cause a lot of vision loss. (Extra credit if you notice that the brightest microaneurysm on the FA is not the same as the most obvious microaneurysm clinically.)

Figure 10. This is why it is good to have an FA before treating near the fovea. The circle represents an estimate of 500 microns from the fovea based on the patient's nerve. The microaneurysms temporal to the fovea (between the arrows) are far enough away to be treatable if you decide to follow ETDRS guidelines. However, you can see from the FA that aggressive treatment of these little devils could shut down the only vessels supplying the entire temporal side of the fovea—you could cause a lot of vision loss. (Extra credit if you notice that the brightest microaneurysm on the FA is not the same as the most obvious microaneurysm clinically.)

Although the ETDRS allowed treatment to within 300 microns of the fovea if necessary, if you really feel that you just have to treat closer than 700 microns, you may want to get a second opinion first. You will find an occasional patient that has a few big leakers near the foveal avascular zone, and gentle treatment directed only at the microaneurysms may fix the problem. In general, however, bad leaks in this area don't tend to respond to laser, especially if the fovea is cystic. You may need to consider intravitreal therapy, if it is available. (Such therapy was not available when the ETDRS was performed, and laser was the only way to try to dry up foveal edema—hence the more desperate treatment guidelines.) Definitely consider getting an OCT, too. Patients may have subtle traction that is keeping the fovea thick, and the vascular changes may be only bit players; ruling traction out first may save a lot of hassle. Remember that spots this close to the fovea will grow—are you sure that everyone will be happy with the results in five years if they spread into the fovea? Finally, never forget that any patient with refractory edema may actually have a bigger problem, such as accelerated hypertension or early renal failure. No perifoveal laser is going to replace nephrons—so think globally before acting locally on juxtafoveal RPE.

The goal of life is to seek a balance between extremes. This is very true in the setting of laser treatment for diabetic macular edema. There is no question that very heavy treatment seems to be effective in eliminating edema (no retina = no edema), but can also create more problems with scotomas, decreased vision, and late complications. Lighter treatment decreases the risks of treatment, but also engenders the risk of permanent damage from incompletely treated macular edema. The best way to judge the needs of an individual patient's retina is experience, and if you end up treating a lot of diabetics you will develop a good sense for this. Until then, take heart—perhaps the most reasonable approach is to be very conservative in your treatments and follow the patients closely, retreating as necessary. There is probably more damage done by overly aggressive treatment of focal disease than by delayed treatment of focal disease. An upcoming chapter will try to give you some idea of what to watch for and when to bail out on patients with difficult-to-control macular disease. But first, a colorful box break followed by a mini-chapter on advanced laser techniques.

Sometimes an Angiogram has a Cheatin' Heart

Although the angiogram is usually your friend, there are times it can deceive you. For instance, patients may have "compensated" leakage on the FA. This means that they can have areas of leakage in the later phases, but that somehow the retina and RPE are able to pump the leakage out fast enough so that there is no secondary swelling of the retina. In other words, the angiogram may indicate there are areas that need to be treated but if you look closely at the retina with your own eyes there is actually no thickening and therefore no "clinically significant" macular edema.

Sometimes these areas of compensated leakage will have subtle thickening on OCT that is not apparent on clinical exam, or there may be early cystic changes on the OCT without any thickening. If these OCT findings are present it may justify treatment, but you must remember that the original ETDRS did not use OCT to determine who gets treated—only the clinical exam. Although treating patients based on a combination of FA and OCT findings alone—without clinically apparent thickening—seems reasonable it is not supported by a randomized trial yet. Proceed with caution.

Another way an angiogram can mess you up is with the diffuse leakage that can occur at the site of previous laser scars. These areas almost always stain into the later phases and you can really chase your tail if you keep hammering laser into these areas thinking that there is still leakage to treat (not to mention the fact that you will create large patches of atrophic retina and RPE). Again, look at the patient. Usually areas of previous laser treatment will be flatter and therefore do not need to be treated—even if they are leaking on the FA. If they are swollen in spite of previous treatment then you and the patient have a problem. If the previous laser is light then you can add some more. If there is a lot of laser you do not want to be beating the proverbial dead horse and blindly keep killing RPE—it may be time to think about other treatments such as intravitreal therapy or to re-evaluate the patient for subtle traction or a systemic problem that is causing trouble.

References and Suggested Reading

1. Fong DS, Strauber SF, Aiello LP, et al. Comparison of the modified Early Treatment Diabetic Retinopathy Study and mild macular grid laser photocoagulation strategies for diabetic macular edema. Arch Ophthalmol. Apr 2007;125(4):469-480.

Folk JC, Pulido JS. Laser photocoagulation of the retina and choroid. San Francisco: American Academy of Ophthalmology, 1997.

Chew EY, Ferris FL III. Nonproliferative Diabetic Retinopathy. In: Ryan SJ. Retina, 4th ed. Philadelphia: Elsevier Mosby, 2006:v.2, pp 1271-1284.

Techniques for scatter and local photocoagulation treatment of diabetic retinopathy: Early Treatment Diabetic Retinopathy Study Report no. 3. The Early Treatment Diabetic Retinopathy Study Research Group. Int Ophthalmol Clin 1987;27:254-64.

Photocoagulation for diabetic macular edema: Early Treatment Diabetic Retinopa-thy Study Report no. 4. The Early Treatment Diabetic Retinopathy Study Research Group. Int Ophthalmol Clin 1987;27:265-72.

Case reports to accompany Early Treatment Diabetic Retinopathy Study Reports 3 and 4. The Early Treatment Diabetic Retinopathy Study Research Group. Int Ophthalmol Clin 1987;27:273-333.

Neubauer AS, Ulbig MW. Laser treatment in diabetic retinopathy. Ophthalmologica 2007;221:95-102.

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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