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In macular edema, the problem stems from blood vessels that are leaky. In PDR, the problem stems from blood vessels that have simply died off. This starts in the periphery and gradually moves toward the center. The dead and dying retina then releases vasoproliferative factors that stimulate new blood vessels to grow (Figure 1).

Figure 1. Ischemic peripheral retina emits vasoproliferative factors into the vitreous.

If the blood vessels simply grew in isolation, without any vitreous to latch onto, they would probably form beautiful branching patterns on the retinal surface—which would largely be of academic interest. Unfortunately, the vitreous is usually firmly attached to the retina in diabetics, and the blood vessels love to grow up into it like kudzu on a trellis (Figure 2).

Ischemic Diabetes Foot Images

Figure 1. Ischemic peripheral retina emits vasoproliferative factors into the vitreous.

Nonperfusion Definition
Figure 2. New vessels grow into the vitreous in response to the vasoproliferative substances. The photograph is a wide-field FA showing extensive peripheral capillary dropout and secondary neovascularization at the border of perfused and non-perfused retina. (Photo courtesy of Raj K. Maturi, M.D.)

All this would be bad enough, but it gets worse. These new blood vessels are quite leaky, and even if they don't hemorrhage, they allow serum components into the vitreous that the vitreous would normally never see. These compounds cause the vitreous to shrink up sooner than it otherwise would. Although vitreous collapse is a normal aging phenomenon, in proliferative retinopathy the contraction process is accelerated and tends to be more vicious. This is a real problem because the vitreous begins to pull on the new vessels (Figure 3).

Figure 3. The vitreous contracts and starts to tug on the new vessels.

Unfortunately, the new vessels are now an extension of the retinal vasculature, and as such, they serve to lock the vitreous onto the retina wherever the blood vessels grow. This means that the shrinking vitreous now begins to tug on both the vessels and the retina. Moreover, connective tissue brought in by the new vessels also tends to shrink, which basically turns the vascular frond into the physiologic equivalent of a power winch that contracts in all directions. The result is that vessels at the surface of the retina are placed under constant tension, and the retina itself can be lifted from the pigment epithelium (Figure 4). If left untreated, the final result of this process is for the entire retina to be yanked off the back of the eye.

Figure 4. Progressive traction from the vitreous and the vessels begins to pull the retina off the RPE.

As this process is evolving, the stretched blood vessels crack open and bleed, subjecting the patient to periodic hemorrhages. The patient notices these hemorrhages as streaks, cobwebs and/ or clouds in their vision. This will usually motivate them to come in for an evaluation if they have been less than diligent in their follow up. Unfortunately, things are usually far advanced by the time the hemorrhages occur. The blood vessels will often be quite extensive and even if they can be controlled with laser, it is likely that there will still be a gradual buildup of traction as the vitreous and connective tissue continue to contract. Such traction may cause anything from mild metamorphopsia (from pulling gently on the posterior pole) to total vision loss (from a tractional retinal detachment). Intermediate problems can include anything from chronic macular edema (due to subtle traction on the macula) to insidious vision loss (from traction on

Busted Blood Vessel With Diabetic Needle

Figure 3. The vitreous contracts and starts to tug on the new vessels.

Broken Blood Vessel The Retina

Figure 4. Progressive traction from the vitreous and the vessels begins to pull the retina off the RPE.

the nerve). If the traction is very severe it may even rip holes in the retina. Once the vacuum-pack seal between the retina and retinal pigment epithelium is broken, the gliotic retina can snap off the back of the eye like a broken garage door spring. These are all Bad Things.

Back in the old days of retinopathy treatment, doctors would shoot at the growing blood vessels on the assumption that the blood vessels themselves were the root of the problem. It quickly became apparent that this approach was worse than useless. Treating the blood vessels alone tends to make them go bananas; they just get revved up by the irritation of the treatment superimposed on the powerful neovascular stimulus created by the dying peripheral retina. Such treatment did not address the more fundamental issue of having an eye full of vasoproliferative substances. Fortunately, there were people who were willing to think in a very open-minded fashion, and these folks observed that patients with lots of peripheral retinal scarring had less active proliferative disease, whether the scarring was from iatrogenic retinal treatment or preexisting ocular conditions. This eventually led them to try using a laser—or a xenon arc, or even focused light from the sun—to destroy the peripheral retina, shutting down the production of vasoproliferative factors and, in turn, shutting down the neovascularization. Apparently the thought of doing this was so counterintuitive that many people thought these pioneers were insane, but they were ultimately vindicated by the success of panretinal photocoagulation as demonstrated by the Diabetic Retinopathy Study. By the way, these last sentences are horribly inadequate to relay the immense effort on the part of the many individuals who have given us this incredible tool to prevent blindness. Every once in awhile, as your foot is racking up numbers on the laser counter, you should think about the broad shoulders upon which we are all standing as we treat diabetics with proliferative disease.

Hunting Down Nonproliferative and Proliferative Retinopathy in Your Patient

Your eternal goal is to try to stop the above chain of events at an early stage before the diabetes can sink too many of its fangs into the retina—before the vessels and fibrovascular tissue have spread all over the place. You should therefore become adept at identifying anything that even remotely suggests the impending arrival of proliferative disease. This means becoming familiar with the various stages of nonproliferative diabetic retinopathy (NPDR). Remember that NPDR can be minimal, mild, moderate or severe (Table 1 shows the standard classification scheme). Severe NPDR is of greatest importance, making it the one you need to be able to recognize unfailingly.

Fortunately, the 4-2-1 rule makes matters relatively easy when it comes to sorting out patients with good-bad retinopathy from those with bad-bad retinopathy. The 4-2-1 part refers to four quadrants of hemorrhages, two quadrants of venous beading or one quadrant of intraretinal microvascular abnormalities

(IRMAs). If a patient has any one of these criteria, then they have severe NPDR. The required amount for each of these findings is defined by the standard photographs used in all of the studies, and you should cram these images into your brain so that you can quickly pick out a patient at risk.

Table 1 / Classification of Diabetic Retinopathy

Level

Definition

Minimal nonproliferative retinopathy

Microaneurysms only

Mild nonproliferative retinopathy

Microaneurysms and one or more of the following:

• Retinal hemorrhage

• Hard exudates

• Nerve fiber layer infarct

Moderate nonproliferative retinopathy

Hemorrhages and microaneurysms > standard photograph 2A in at least one quadrant and one or more of the following:

• Nerve fiber layer infarct

• Venous beading

• Intraretinal microvascular abnormality

Severe nonproliferative retinopathy

One of the following:

• Hemorrhages/microaneurysms > standard photograph 2A in all 4 quadrants

• Venous beading in at least 2 quadrants

• IRMA > standard photograph 8A

Proliferative retinopathy

Neovascularization on the disc or elsewhere

High-risk proliferative retinopathy

One or more of the following:

• Neovascularization of the disc > 1/4 disc area

• Any neovascularization of the disc and vitre-ous/preretinal hemorrhage

• Neovascularization > 1/2 disc area with vitre-ous/preretinal hemorrhage

Advanced proliferative retinopathy

Proliferative retinopathy with tractional retinal detachment or with extensive vitreous hemorrhage

(Reproduced, with permission, from Fong DS, Ferris FL, Focal Points: Clinical Modules for Ophthalmologists, "Practical Management of Diabetic Retinopathy," American Academy of Ophthalmology, 2003.)

(Reproduced, with permission, from Fong DS, Ferris FL, Focal Points: Clinical Modules for Ophthalmologists, "Practical Management of Diabetic Retinopathy," American Academy of Ophthalmology, 2003.)

Figure 5. (Left) ETDRS Standard Photograph 2a, showing severe hemorrhages and microaneurysms (remember—you need these in four quadrants to get severe NPDR). (Courtesy of the Early Treatment Diabetic Retinopathy Study Group)

Figure 5. (Left) ETDRS Standard Photograph 2a, showing severe hemorrhages and microaneurysms (remember—you need these in four quadrants to get severe NPDR). (Courtesy of the Early Treatment Diabetic Retinopathy Study Group)

Diabetic Photograph

Figure 6. (Right) ETDRS Standard Photograph 6a, the criterion for going from mild to moderate venous beading. Notice that you don't need a lot. If you can see obvious venous beading in a patient, then it's bad (but you need two quadrants for severe NPDR). Also, be sure that it is venous beading and not just venous caliber changes. With true venous beading the beaded section must be wider than the normal caliber and because venous beading tends to be a late finding you should also judge it by the company it keeps-there should be other worrisome findings as well. (Courtesy of the Early Treatment Diabetic Retinopathy Study Group)

Figure 7. (Below) ETDRS Standard Photograph 8a. The circles show the odd, curlicue shape of IRMA. (Courtesy of the Early Treatment Diabetic Retinopathy Study Group)

Figure 7. (Below) ETDRS Standard Photograph 8a. The circles show the odd, curlicue shape of IRMA. (Courtesy of the Early Treatment Diabetic Retinopathy Study Group)

Diabetic Retinopathy Irma

If memorizing the scheme is too painful, you can simplify it this way: if you look in and you can see obvious venous beading and/or definite IRMA, then the patient has severe NPDR or something very close to it. See the blue box if you think they have severe NPDR based on hemorrhages alone...

Although the presence of hemorrhages is one of the criteria for severe NPDR, as a practical matter it can be a less reliable predictor in clinical practice. Hemorrhages, like glory, can be fleeting, and they are not quite as dependable as hardcore venous beading and IRMA.1 Just review the chapter on differential diagnosis to see the many ways hemorrhages may be unrelated to factors that cause proliferative disease. Then look in Chapter 16, where hemorrhages can resolve with institution of good systemic control. Finally, remember how patients on blood thinners may have very dramatic hemorrhages that have nothing to do with NPDR. The real point here is that if you think a patient has NPDR solely because of four quadrants of hemorrhages, and if you are going to treat them with laser, you should be sure they don't have hemorrhages for other reasons.

When it comes to hunting down evidence of severe NPDR, hemorrhages and venous beading tend to be fairly obvious. IRMAs, on the other hand, can be a bit trickier to identify. IRMAs are tiny, and are usually located in little patches outside the arcades, so it is something that you have to look for with your 90-di-opter lens (or 78-diopter or whatever fundus-o-rama lens is being marketed this year by the lens manufacturers). You will need to have the patient look in different directions, similar to the indirect ophthalmoscope exam, and you will need to perfect your ability to use an indirect slit lamp lens for this purpose—something that has to be mastered in order to do a thorough exam for diabetic retinopathy.

Late-Seventies programmed-learning moment: What is a skill that has to be mastered in order to do a thorough exam for diabetic retinopathy?

a. Understanding the conoid of Sturm b. Understanding phacodynamics c. Understanding Medicare d. Using a slit lamp indirect lens to study the midperiphery e. Do you see why the Seventies were so much fun?

It is really hard to manage diabetics without being able to do this.

When hunting for IRMAs you are looking for fine, irregular vessels that seem to be within or just at the surface of the retina—they do not follow any normal flow pattern and tend to meander around in a tiny area. Sadly, almost every attempt to reproduce photos of IRMAs is foiled by the limitations of the printing process—Figure 8 is a blowup of the standard ETDRS figure, so you get some idea of what you are looking for.

Why bother with this? Eyes with severe NPDR have as much as a 50% chance of developing some degree of PDR within one year, and perhaps a 15% chance of developing high-risk PDR. These averages are from the ETDRS—your mileage may vary with specific patients. If a patient has a long history of good control and very slow progression of their retinopathy, then their risk is much less. If they have poor control and are rapidly going to severe NPDR, then they are far more likely to get into trouble. The point is that knowing the stages of NPDR allows you to determine the patient's risk for progression to PDR and to decide how closely to follow the patient. Staging the patient may also help you decide whether they need panretinal photocoagulation before they get a chance to develop proliferative disease. Vide infra.

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