Intraretinal microvascular abnormalities may be a precursor to retinal neovascularization. Diabetic retinopathy is either proliferative (with neovascularization) or non–proliferative (without ovascularization). 3, 4 Diabetic maculopathy is considered a separate entity, consisting of dot and blot hemorrhages, hard exudates and CSME. 5.

Diabetic maculopathy calls for laser treatment only in cases involving CSME. The surgeon applies argon laser photocoagulation to all leaking microaneurysms more than 500µm from the center of the foveal avascular zone. If fluorescein angiography reveals that microaneurysms are the cause of CSME, they receive focal photocoagulation. If diffuse leakage causes CSME, the surgeon applies photocoagulative burns in a grid pattern. 6–8. The aim is to preserve the remaining vision.

Cases of high–risk proliferative retinopathy when vision may drop to 5/200 or worse as well as iris neovascularization warrant panretinal photocoagulation. Argon laser burns destroy areas of hypoxic retina from just beyond the vascular arcades of the posterior pole to the far periphery. 4, 9 The eye’s oxygen demand decreases, and the neovascularization regresses. Prompt treatment of high–risk proliferative retinopathy or iris neovascularization reduces the risk of severe vision loss by 50 percent. 4.

Hypertensive Retinopathy
Systemic hypertensive vascular changes can affect the retinal vessels. 10 Hypertensive retinopathy initially involves narrowing of the retinal arterioles. In prolonged systemic hypertension, the retinal vessels become arteriolosclerotic. Fibrosis in the vessel wall and perivascular tissue causes further narrowing.

As the sclerotic process advances, the arterioles change color, first exhibiting increased luster, then changing to copper, then silver. Ultimately the arterioles take on a cord like appearance with no apparent bloodstream. They’ll also show focal constriction representing sclerosis from prolonged diastolic pressures of 110mm Hg or higher. 11.

You’ll also see arteriovenous crossing constrictions. As the sclerotic arteriole crosses a weak–walled venule, it compresses that venule. This impedes drainage and can contribute to a branch vein occlusion.

Later stages of hypertensive retinopathy will reveal flame–shaped hemorrhages in the nerve fiber layer. Arteriolar occlusion with subsequent cotton wool spots will also occur within the nerve fiber layer.

Macular edema may develop in hypertensive retinopathy, but tends to be self–limiting, and is amenable to photocoagulation. Edematous residue in the form of a macular exudative star signals advanced, long–standing hypertension. Disc edema often accompanies malignant hypertension. We don’t fully understand its cause. In some cases it may be due to increased intracranial pressure. Edema of the disc and surrounding retina, often with an accompanying macular star, is a medical emergency.

Managing hypertensive retinopathy involves little direct intervention. If there’s persistent macular edema, refer the patient for photocoagulation. Also refer to a primary care physician to manage the hypertension.