SIGNS AND SYMPTOMS
A microvascular disease that primarily affects the capillaries, diabetes mellitus affects the eye by destroying the vasculature in the conjunctiva, retina and central nervous system. Patients may present with histories of long-standing injected bulbar conjunctivae along with systemic complaints of weight loss despite larger than normal appetite (polyphasia), abnormal thirst (polydypsia) and abnormally frequent urination (polyuria).

Fluctuating visual acuity secondary to unstable blood sugar is a common ocular sign. Swelling within the crystalline lens results in large sudden shifts in refraction as well as premature cataract formation. Changes in visual acuity will depend upon the severity and stage of the disease.

In the retina, weakening of the arterioles and capillaries may result in the characteristic appearance of intraretinal dot and blot hemorrhages, exudates, intraretinal microvascular abnormalities (IRMA) microaneurysms, edema and cotton wool infarcts. Proliferative diabetic retinopathy is the result of severe vascular compromise and is visible as neovascularization of the disc (NVD), neovascularization elsewhere (NVE) and neovascularization of the iris (NVI, or rubeosis irides). Neurological complications include palsies of the third, fourth and sixth cranial nerves as well as diabetic papillitis and facial nerve paralysis.

PATHOPHYSIOLOGY
Diabetes mellitus is a genetically influenced group of diseases that share glucose intolerance. It is characterized as a disorder of metabolic regulation as a result of deficient or malfunctioning insulin or deficient or malfunctioning cellular insulin receptors.

Biochemistry involving the formation of sorbitol plays a role in the destruction of pericytes, which are cells that support the vascular endothelium. As the supportive pericytes perish, capillary endothelium becomes compromised, resulting in the vascular leakage of blood, protein and lipid. This, in combination with thickened, glucose-laden blood, produces vascular insufficiency, capillary nonperfusion, retinal hypoxia, altered structure and decreased function. The formation and release of vasoproliferative factors which play a role in the genesis of retinal neovascularization are poorly understood.

MANAGEMENT
When you suspect ocular sequelae of diabetes mellitus in an undiagnosed individual, either you or the patient's physician should order a fasting blood glucose (FBS), glycosylated hemoglobin or oral glucose tolerance test (OGTT).

Most non-vision threatening sequelae of diabetes resolve spontaneously over the course of weeks to months following medical control. In cases where there are large refractive changes, patients may require a temporary spectacle prescription until the refraction stabilizes. The most important element of

MANAGEMENT is education so that patients are informed that they may eventually need to change their spectacle lenses.

When retinopathy threatens the macula or when new blood vessels proliferate, refer for laser photocoagulation. The Diabetic Retinopathy Study (DRS) has conclusively proven that panretinal photocoagulation was successful in reducing the risk of severe vision loss in high risk patients. It defined the high risk characteristics as: (1) Neovascularization of the optic disc (NVD) one-quarter to one-third of a disc diameter in size and (2) Neovascularization elsewhere (NVE) with any vitreous hemorrhage.

If the patient exhibits either of these high risk characteristics, refer him or her to a vitreoretinal specialist.

The Early Treatment of Diabetic Retinopathy Study (ETDRS) has shown that focal/grid laser photocoagulation reduced the risk of moderate vision loss in patients with clinically significant macular edema, defined as: (1) retinal thickening at or within 500 microns (one-third of a disc diameter) of the center of the foveola, (2) exudate at or within 500 microns of the center of the foveola only if associated with retinal thickening, or (3) an area of retinal thickening one disc diameter or greater in size, within one disc diameter of the foveola.

If you observe any of these signs, regardless of the acuity, refer the patient to a retinal specialist. Referral is also indicated if you suspect clinically significant macular edema but are having difficulty visualizing the macula or edema.

CLINICAL PEARLS

• Clinically significant macular edema is unrelated to acuity and can exist in the presence of 20/20 vision. It can only be identified through observation using stereoscopic indirect biomicroscopy (60D, 78D, 90D Hruby or three-mirror lens).

• Fluorescein angiography is only used for treatment. It identifies the areas of leakage that require focal grid laser photocoagulation. With respect to diabetes, it is not a tool for diagnosis. Angiography is not required for treating proliferative disease since PRP does not require precise aiming of the laser.

• The development of diabetic retinopathy is time-dependent. Even in the face of optimal blood sugar control, patients with long-standing disease can be expected to eventually develop some form of retinopathy.

Other reports in this section

• Posterior Vitreous Detachment
• Tractional Retinal Tears
• Epiretinal Membrane
• Diabetic Retinopathy
• Lattice Degeneration
• Retinal Vein Occlusion
• Retinal Artery Occlusion
• Macular Degeneration
• Toxoplasmosis
• Choroidal Melanoma
• Acquired Retinoschisis
• Hollenhorst Plaque
• Idiopathic Central Serous Chorioretinopathy
• Macular Hole
• Presumed Ocular Histoplasmosis Syndrome
• Retinal Macroaneursym
• Retinitis Pigmentosa
• Retinal Detachment
• Hypertensive Retinopathy
• Retinal Pigment Epithelium (RPE) Detachment
• Papillophlebitis
• Ocular Ischemic Syndrome
• Coats’ Disease and Leber’s Miliary Aneurysm