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Diabetic retinopathy includes microaneurysms, intraretinal hemorrhage, exudates, macular edema, macular ischemia, neovascularization, vitreous hemorrhage, and traction retinal detachment. Symptoms may not develop until late in the disease. Diagnosis is by funduscopy; further details are elucidated by fluorescein angiography and optical coherence tomography. Treatment includes control of diabetes and BP and ocular laser photocoagulation, intravitreal injection of drugs, vitrectomy, or a combination.

Pathophysiology

Diabetic retinopathy is a major cause of blindness. The degree of retinopathy is highly correlated with

• Duration of diabetes
• Blood glucose levels
• Blood pressure levels

Pregnancy can impair blood glucose control and thus worsen retinopathy.

Nonproliferative retinopathy: (also called background retinopathy) develops first and causes increased capillary permeability, microaneurysms, hemorrhages, exudates, macular ischemia, and macular edema (thickening of the retina caused by fluid leakage from capillaries).

Proliferative retinopathy: develops after nonproliferative retinopathy and is more severe; it may lead to vitreous hemorrhage and traction retinal detachment. Proliferative retinopathy is characterized by abnormal new vessel formation (neovascularization), which occurs on the inner (vitreous) surface of the retina and may extend into the vitreous cavity and cause vitreous hemorrhage. The neovascularization is often accompanied by preretinal fibrous tissue, which, along with the vitreous humor, can contract, resulting in a traction retinal detachment. Neovascularization may also occur in the anterior segment of the eye on the iris, which can result in neovascular membrane growth in the angle of the eye at the peripheral margin of the iris, leading to neovascular glaucoma. Vision loss with proliferative retinopathy may be severe.

Clinically significant macular edema can occur with nonproliferative or proliferative retinopathy and is the most common cause of vision loss due to diabetic retinopathy.

Symptoms and Signs

Nonproliferative retinopathy: Vision symptoms accompany macular edema or macular ischemia. However, patients may be unaware of vision loss. The first signs of nonproliferative retinopathy are

• Capillary microaneurysms
• Dot and blot retinal hemorrhages
• Hard exudates
• Cotton-wool spots (soft exudates)

Diabetic Retinopathy (Nonproliferative)

Cotton-wool spots are areas of microinfarction that lead to retinal opacification; they are fuzzy-edged and white and obscure underlying vessels. Hard exudates are discrete, yellow, and generally deeper than retinal vessels and suggest retinal edema.

Signs in later stages are

• Macular edema (seen on slit-lamp biomicroscopy as elevation and blurring of retinal layers)
• Venous dilation and intraretinal microvascular abnormalities

Proliferative retinopathy: Symptoms may include blurred vision, black spots or flashing lights in the field of vision, and sudden, severe painless vision loss. Some of these symptoms may be caused by vitreous hemorrhage or traction retinal detachment.

Proliferative retinopathy, unlike nonproliferative retinopathy, causes fine preretinal capillaries (newly developed capillaries) to appear on the optic nerve or retinal surface. Macular edema or retinal hemorrhage may be visible on funduscopy.

Diabetic Retinopathy (Proliferative)

Diagnosis

• Funduscopy
• Fluorescein angiography
• Sometimes optical coherence tomography

Diagnosis is by funduscopy. Fluorescein angiography is used to determine the extent of damage, to develop a treatment plan, and to monitor the results of treatment. Optical coherence tomography is also useful to assess severity of macular edema and treatment response.

Screening: Because early detection is important, all patients with diabetes should have annual dilated ophthalmologic examination. Pregnant patients with diabetes should be examined every trimester. Vision symptoms are indications for ophthalmologic referral.

Treatment

• Control of blood glucose and BP
• For macular edema, focal laser and possibly vitrectomy or intravitreal drugs
• For high-risk or complicated proliferative retinopathy, panretinal laser photocoagulation and sometimes vitrectomy

Control of blood glucose and BP are critical; intensive control of blood glucose will slow progression of retinopathy. Clinically significant diabetic macular edema is treated with focal laser. Intravitreal injection of triamcinolone Some Trade Names
ARISTOCORT
KENACORT
KENALOG
NASACORT
Click for Drug Monograph
, as well as anti-vascular endothelial growth factor (VEGF) drugs, may help in more severe cases. Vitrectomy can also help in recalcitrant diabetic macular edema. In select cases of severe nonproliferative retinopathy, panretinal laser photocoagulation may be used; however, most patients can be followed closely until proliferative retinopathy develops.

Proliferative diabetic retinopathy with high-risk characteristics of vitreous hemorrhage, extensive preretinal neovascularization, or anterior segment neovascularization/neovascular glaucoma, should be treated with panretinal laser photocoagulation. This treatment reduces the risk of severe vision loss significantly.

Vitrectomy can help to preserve, and often restore, lost vision, with any of the following:

• Vitreous hemorrhage that persists for 3 mo
• Extensive preretinal membrane formation
• Traction retinal detachment

Prevention

Control of blood glucose and blood pressure are critical; intensive control of blood glucose will delay onset of retinopathy.

Last full review/revision December 2008 by Sunir J. Garg, MD

Content last modified December 2008