Diabetic macular edema, or clinically significant macular edema, exists when there is leakage in or close to the macula. When the macula becomes swollen, the vision worsens (despite glasses). This is the most common problem in patients with diabetic retinopathy. Usually, laser photocoagulation is employed to treat the leaking blood vessels. This has been the mainstay of treatment since the late 1970's.  The laser needs to be repeated just as one needs to periodically weed a garden.  New microaneuryms can develop that need to be treted.  Occasionally, residual macular edema remains.  Intravitreal injection of steroids has been found to be very useful and is another way to treat macular edema.  Kenalog (triamcinolone acetonide) as been very effective in treating these more difficult cases.  There is commonly tremendous reduction of swelling and a noticeable improvement in vision.

A smaller percentage of patients may develop proliferative diabetic retinopathy.  Here, there is such poor blood supply to the retina, that the retina becomes ischemic (lacks sufficient oxygen) and the demand for oxygen by the retina exceeds the actual supply due to the compromised blood circulation.  Abnormal blood vessels now grow on the surface of the retina and on other structures.  This can lead to a diabetic retinal detachment or neovascular glaucoma; both of which can lead to blindnesss.  The best way to control proliferative diabetic retinopathy is with laser to the peripheral retina (in contrast to treating diabetic macular edema).  If enough panretinal photocoagulation (aka PRP) is done, the neovascularization may shrink up and go away.   This laser does not commonly need to be repeated if enough is performed at the outset. 

Panretinal photocoagulation usually works very well.  When the eye is ischemic, the eye produces Vascular Endothelial Growth Factor, aka VEGF.  VEGF is responsible for the growth and maintainence of the abnormal blood vessels called neovascularization.  Remember that VEGF is produced with the eye is not getting enough oxygen.  We do not know how to increase oxyge delivery to the eye.  Each laser burn actually "kills" retinal tissue.  After 1-2 thousand burns to the peripheral retina, a certain percentage of retina has been "killed" and no longer requires oxygen.  By reducing the demand, the oxygen supply becomes adequate, VEGF is no longer produced and the neovascular process has stablized or reversed.

Intravitreal injection of Avastin or other VEGF inhibitors may also play a role in reversing or stabilizing patients with proliferative disease, but at this time, it is unclear if the injections are long lasting in this scenario. 

Once in a while, patients develop traction or diabetic retinal detachments or may have a vitreous hemorrhage.  Surgery may be the only alternative at this point.  A vitrectomy, membrane stripping and PRP can be effective in preventing complete blindness.

Randall V. Wong, M.D.

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