The eye is frequently involved in diabetes mellitus, and ocular symptoms, which occur in 20% to 40% of diabetics at the clinical onset of the disease, may be a presenting manifestation of this common cause of blindness. Visit: Diabetes Mellitus

Diabetic Retinopathy:   Normal histology and diseases of the retina : click here

Diabetic retinopathy usually follows 10 to 20 years after the onset of diabetes, and its prevalence increases with the duration of the disease (75% to 90% of patients have retinal changes after 25 years of diabetes).

The incidence of diabetic retinopathy is increasing because of the improved life expectancy of treated diabetics.

 Diabetic retinopathy under the age of 10 is rare, and most cases are over the age of 50 years.

Women are not only more prone to diabetes than men, but also develop diabetic retinopathy more frequently.

The retinopathy does not seem to be closely related to the severity of the diabetes nor to the cause of it, but similar to other delayed lesions in diabetes mellitus, the retinopathy is an outcome of vascular disease. Diabetic retinal microangiography correlates directly with diabetic glomerulosclerosis.

Retinal ischemia, which can account for most features of diabetic retinopathy, including the cotton wool spots, capillary closure, microaneurysms, and retinal neovascularization, may result from narrowing or occlusion of retinal arterioles (as from arteriosclerosis or platelet and lipid thrombi), or from atheromatosis of the central retinal or ophthalmic arteries.

The progression of diabetic retinopathy is retarded by treating the retina in multiple sites by laser photocoagulation.

The retinopathy of diabetes is characterized by nonproliferative and proliferative stages.

Nonproliferative diabetic retinopathy:

Nonproliferative diabetic retinopathy exhibits venous engorgement, small hemorrhages (“dot and blot hemorrhages”), capillary microaneurysms, and exudates.

These lesions usually do not impair vision, unless associated with macular edema.

The retinopathy begins at the posterior pole, but eventually may involve the entire retina.

The first discernible clinical abnormality in nonproliferative diabetic retinopathy is engorged retinal veins, with localized sausage-shaped distension, coils, and loops.

This is followed by small hemorrhages in the same area, mostly in the inner nuclear and outer plexiform layers.

With time, “waxy” exudates accumulate, mostly close to microaneurysms.

The retinopathy of the elderly diabetic frequently displays numerous exudates (exudative diabetic retinopathy), while this is not a feature in juvenile diabetics.

Because of the hyperlipoproteinemia of diabetics, the exudates are rich in lipid, and hence appear yellowish (“waxy” exudates)’

Capillary microaneurysms appear in areas of poor retinal vascular perfusion and are best seen in the living eye by taking numerous sequential photographs of the retinal fundus after an intravenous injection of flourescein (flourescein angiograph).

Capillary microaneurysms can also be seen in flat preparations of the retina.

Proliferative diabetic retinopathy:

After many years the retinopathy becomes proliferative.

Delicate new blood vessels grow with fibrous and glial tissue toward the vitreous humor.

Neovascularization of the retina is a prominent feature of diabetic retinopathy and of other conditions caused by retinal ischemia.

Chronic hypoxia is presumed to provoke the secretion of a diffusible angiogenic factor by retinal cells.

Tortuous new vessels first appear on the surface of the retina and optic nerve head and then grow into the vitreous cavity.

The newly formed friable vessels bleed easily, and the resultant vitreal hemorrhage obscures vision by impairing the ability of light to reach the retinal photoreceptors.

The neovascularization is associated with a proliferation and migration of astrocytes, which grow around the new vessels to form delicate white veils (gliosis).

The proliferating, preretinal, fibrovascular, gliotic tissue contracts, often causing retinal detachment and blindness.

In young diabetics with marked acidosis the retinal vessels are light pink to yellowish because of hyperlipidemia (lipemia retinalis).

Frequently, features of hypertensive and arteriosclerotic retinopathy are associated with diabetic retinopathy. Usually both eyes are affected simultaneously and more or less equally.

In diabetes mellitus blindness results when the macula is involved in the retinopathy, but it also follows vitreous hemorrhage, retinal detachment and glaucoma.

Once blindness ensues it heralds an ominous feature for the patient, since the average life expectancy is then less than 6 years, and only one-fifth of blind diabetics survive 10 years.

Thickened Basement Membrane:

In patients with diabetes the basal lamina of the retinal capillaries and of the pigmented epithelium of the ciliary body is frequently duplicated and is considerably thicker than normal. The thickened basement membrane is identical to that in the kidney and other locations in diabetics.

Diabetic Iridopathy:

In diabetics with severe retinopathy, a fibrovascular layer frequently grows along the anterior surface of the iris and in the anterior chamber angle.

Because such iris neovascularization (“rubeosis iridis”) is a feature of several conditions associated with retinal ischemia, it is believed to be due to an angiogenic factor produced by the ischemic retina.

The fibrovascular membrane leads to adhesions between the iris and the cornea (peripheral anterior synechiae) and between the iris and lens (posterior synechiae), while traction by the fibrovascular membrane pulls the iris pigment epithelium around the pupillary margin (ectropion uveae).

The friable new vessels on the iris bleed easily and cause hyphema.

Similar to diabetic retinopathy, and usually involving both eyes, iris neovascularization is clinically important because it frequently culminates in a blind painful eye due to a secondary glaucoma (“neovascular glaucoma”).

The elevated aqueous sugar level that accompanies hyperglycemia leads to glycogen storage in the pigmented epithelium of the iris, a phenomenon analogous to that produced in the renal tubules by glycosuria (Armanni-Epstein phenomenon).

When tissue sections of diabetic eyes are processed in the usual manner, the pigment epithelium of the iris sometimes contains numerous vacuoles that impart a lacy appearance. The vacuoles result from the loss of glycogen in the preparation of tissue sections.

The glycogen storage within the pigment epithelium of the iris is thought to account for the scattering of the iris pigment that is observed clinically in diabetic irises.

Diabetes and the lens:

In juvenile diabetics (15 to 25 years old) and, exceptionally, in diabetic infants a blanket of white needle-shaped opacities collects in both crystalline lenses immediately beneath the anterior and posterior lens capsule. These opacities, which resemble snowflakes, coalesce within a few weeks in adolescents, and within days in children, until the whole lens becomes opaque. 

The so called sterile cataracts occur in elderly diabetics at an earlier age than in the general population and progress more rapidly to maturity.

A sudden temporary myopia, caused by an increase in the refractive power of the lens, may be the presenting manifestation of diabetes.

The increased sorbitol content of the lens causes imbibition of water and an enlargement of the lens.

Other ophthalmic manifestations:

Diabetics are at increased risk for the inflammation of the anterior segment of the eye, phycomycosis (mucormycosis) of the orbit, and primary open-angle glaucoma.

Diabetics are also prone to unequal, irregular-shaped pupils that react to accommodation, but not to light (Argyll Robertson pupil).

Cranial nerve palsies, especially of the oculomotor nerve, are seen.

Some individuals with longstanding diabetes develop a keratopathy that is characterized by recurrent epithelial erosions, and that is believed to be due to an impaired corneal innervation.