Diabetic Retinopathy

[Doctor325]

Diabetic Retinopathy

Diabetes is a common disease and many affected patients have vision problems. In fact, diabetics are twenty times more likely to go blind than the general population. Diabetic retinopathy is the term used to describe the retinal damage causing this visual loss. Diabetics have a high prevalence of retinopathy, and one out of every five patients with newly diagnosed diabetes will also show signs of retinopathy on exam.

Mechanism of Vessel Breakdown


How are the eyes affected? Basically, diabetes is a disease of blood vessels. With large amounts of glucose coursing through the circulatory system, a glycosylation reaction occurs between the sugar and the proteins that make up the vessel walls. Over time, this glycosylation promotes denaturing of collagen protein within the walls, creating capillary thickening and eventually, wall breakdown.

While this process occurs throughout the entire body, the microvasculature of certain organs, such as the kidneys and eyes, are more susceptible to damage. Along these lines, a good predictor of microvasculature damage in the diabetic eye is prior evidence of renal microvasculature disease as measured by proteinurea, elevated BUN, and creatinine.

Because vessel damage accumulates over time, the most accurate predictor of retinopathy is duration of diabetes. After 10 years, more than half of patients will show signs of retinopathy, and after 15 years this number increases to nearly 90%. The relative control of glucose during this time is also important, and studies have shown that patients who maintain lower hemoglobin A1C levels have delayed onset and slower progression of disease. Additional risk factors include smoking, hypertension, and pregnancy.





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[Doctor325]

Two Types of Retinopathy

It is useful to divide patients into two categories of retinopathy.
A. Nonproliferative diabetic retinopathy (NPDR)

Most patients (95%) have NPDR. This is the earliest stage of retinopathy and it progresses slowly. Because so many diabetic patients have NPDR, this stage is commonly described as “background retinopathy.” The earliest signs of retinal damage arise from capillary wall breakdown, seen on the fundus exam as vessel microaneurysms. Injured capillaries can leak fluid into the retina and the aneurysms themselves can burst, forming “dot-and-blot hemorrhages.”

Dot-blot hemorrhages look small and round because they occur in the deep, longitudinally-oriented cell layers of the retina. This contrasts with the “flame hemorrhages” of hypertension that occur within the superficial ganglion nerve layer, and thus spread horizontally.

With worsening retinopathy and vessel damage, the retina begins to show early signs of ischemia. Cotton-wool spots, seen with hypertension and stasis, are gray spots with soft edges that indicate ischemia/infarction of the superficial retinal nerve fibers. As vessel damage progresses, you can also see beading of the larger retinal veins and other vascular anomalies.

B. Proliferative Retinopathy

With ongoing injury to the retinal vasculature, there eventually comes a time when the vessels occlude entirely, shutting down all blood supply to areas of the retina. In response, the ischemic retina sends out chemicals that stimulate growth of new vessels. This new vessel growth is called neovascularization, and is the defining characteristic of proliferative retinopathy. Far fewer patients have proliferative retinopathy, which is fortunate as this stage can advance rapidly with half of these patients going blind within five years if left untreated. The mechanism and complications of neovascularization merit study, so let’s take a closer look.
The Mechanism of Neovascularization


With complete vessel occlusion, parts of the retina become starved for nourishment. The ischemic retina responds by releasing angiogenic molecules like VEGF to promote new vessel growth. These new vessels serve to bypass the clogged arteries in order to resupply the starved retina

.

A collateral blood supply seems like a great idea, but unfortunately there is a problem. The newly formed vessels are abnormal in both appearance and function. The new vessels are friable and prone to leaking. They also grow in the wrong place, spreading and growing along the surface of the retina. They can even grow off the retina, sprouting up into the vitreous fluid. The vitreous is mostly water, but it also contains a lattice framework of proteins that the new vessels can adhere to. With vitreous movement or contraction, these new connections pull on the retina and the traction can lead to retinal detachment. Since the vessels are also weak, any vitreous traction can break the vessels and create sudden hemorrhaging with subsequent vision loss as the eye fills with blood. Finally, the new vessels can regress and scar down, creating massive traction on the retina underneath.

Neovascularization isn’t just limited to the retina, but can also occur on the iris itself. NVI (neovascularization of the iris) is an ominous sign, as the new vessels can cover the trabecular meshwork and create a sudden neovascular glaucoma.



Macular Edema
Despite the neovascularization phenomenon and its potential for detachments and hemorrhage, the most common cause of blindness in diabetic patients is from macular edema. This occurs when diffuse capillary and microaneurysm leakage at the macula causes the macular retina to swell with fluid.

Macular edema occurs in about 10% of patients with diabetic retinopathy and is more common with severe retinopathy. On exam the macula looks cloudy and mildly elevated, and you can see past evidence of edema in the form of yellow-colored “hard exudates”. These exudates are fatty lipids that are left behind after past macular swelling subsides, similar to a dirt ring in a bathtub.



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[Doctor325]

Treatment of DR "diabetic retinopathy"


Preventative medicine with tighter control of glucose is the ideal treatment, but for worsening symptoms, surgical treatment is necessary. The two main surgeries are laser treatment and vitrectomy.

Laser Treatment

In cases of macular edema, an argon laser can be used to seal off leaking vessels and microaneurysm in the retina by burning them. If the leakage or microaneurysm is small and well-defined, it can be selectively sealed off. With larger areas of leaking capillaries, such as diffuse macular edema, the laser can lay down a “grid photocoagulation” pattern over the entire area.

With advanced retinopathy and neovascularization,
a different approach is taken. Instead of individually targeting vessels, PRP (pan-retinal photocoagulation) is performed. With PRP, the ophthalmologist burns thousands of spots around the peripheral retina. This destroys the ischemic retina, decreasing the angiogenic stimulus, and commonly leads to regression and even the complete disappearance of the new vessels. This treatment may seem drastic, but it has proven to be effective.

Naturally, there are side effects, with peripheral vision loss and decreased night vision (from the rod photoreceptor loss), but this is acceptable if the central vision is saved. I’ve never seen anyone actually complain of decreased vision, but it’s possible and should be stressed during consent.





Vitrectomy

A vitrectomy may also need to be performed and is often done in conjunction with other surgeries. This surgery involves removing the vitreous humor from the eye and replacing it with saline. This allows removal of hemorrhaged blood, inflammatory cells, and other debris that may obscure the visual axis. While removing the vitreous, the surgeon also removes any fine strands of vitreous attached to the retina in order to relieve traction that might have, or will, cause a detachment.


Conclusion


As you can see, diabetic retinopathy is a big problem as a large percentage of our patients have diabetes. Retinal vessel damage leads to edema, and vessel occlusion stimulates neovascularization that can lead to trouble. Fortunately, better glucose control and surgical treatments have significantly decreased the incidence of visual loss in these patients.



Retinal Detachments

A retinal detachment is an abnormal separation between the sensory retina and the underlying RPE and choroid plexus. If you remember from the anatomy lecture, the outer third (the part furthest from the vitreous) of the retina gets its nourishment primarily from the underlying choroid - with a detachment, the photoreceptor layer loses its blood supply and becomes ischemic. The macular retina is especially susceptible to this damage.

The prognosis for patients with retinal detachments depends upon the quickness to treatment; patients with detachments that involve the macula have much worse outcomes.



Risk Factors and Epidemiology

Up to six percent of the general population have retinal breaks of some kind, though most of these are benign atrophic holes. The actual incidence of retinal detachment is only 1 in every 10,000 people. Relative risk is equal between men and women, with higher rates in those of Jewish descent and decreased risk in black populations. When looking at patients who already have retinal detachments, you begin to see some interesting trends. Many of these patients are myopic (near-sighted). Myopic eyes are physically larger and longer than normal eyes and have thinner retinas at the periphery. This thin retina is more likely to break, forming small holes and tears that may progress to a detachment. Up to 35 percent of patients with retinal detachments develop them after another eye surgery – typically a cataract extraction. Finally, traumatic sports such as boxing, football, and bungee-jumping predispose younger people to forming detachments.






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