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In Focus |
Out of Sight
Retinopathy and other ophthalmic complications cost diabetics their vision
Diabetic individuals are 25 times more likely to become blind because of complications like diabe-tic retinopathy, diabetic maculopathy, diabetic cataracts, and glaucoma, which may come about singly or in combination. Diabetic retinopathy is the most frequent cause of new cases of blindness in persons 20 to 74 years of age. It is also usually present in 21 percent of newly diagnosed diabetics.
Diabetic retinopathy is either nonproliferative (NPDR) or proliferative (PDR). Nonproliferative diabetic retinopathy usually appears late in the first decade or early in the second decade of the disease. Almost all patients who have had diabetes mellitus for more than 20 years are stricken with NPDR.
NPDR is characterized by retinal vascular aneurysms, blot hemorrhages, and cotton wool spots. The mild form usually progresses, showing observable patho-logies like changes in vein caliber, intra-retinal vascular abnormalities, numerous microaneurysms, and hemorrhages. NPDR directly results from ischemia due to various pathologic processes beginning with loss of retinal pericytes, increased retinal vascular permeability, alterations in retinal blood flow, and abnormal retinal microvasculature.
Angiogenesis and neovascularization characterize PDR. These newly formed vessels can be seen anywhere along the optic nerve or macula or both. Rupture of these vessels usually result in vitreous hemorrhage and fibrosis, both of which contribute greatly to retinal detachment. In many instances, glaucoma may also present. While NPDR's progression to PDR cannot be fully ascertained, it is established that pregnancy, puberty, and cataract surgery can hasten the process.
Although PDR and NPDR cause ha-voc on the various eye structures, it is macular edema or retinal thickening that primarily leads to blindness. Better known as diabetic maculopathy, the condition stems from leaking microaneurysms at the outer plexiform layer of the eye particularly in areas riddled with exudates and lacking in capillaries.
The incidence and severity of macular edema depend on several factors. The most pressing would be severity and duration of diabetes. Other factors are persistently high glycosylated hemoglobin levels, proteinuria, and poor blood pressure and blood sugar control.
The Diabetes Control and Complications Trial (DCCT) showed that intensive insulin therapy prevented the development of retinopathy by 27 percent among diabetics who still had not developed the complication. Among those with overt nephropathy, progression of retinopathy was reduced by 34 to 76 percent. The DCCT said these outcomes were achieved by tight glucose control-lowering the HbA1c from eight to 7.2 percent. The DCCT also reported a 25-percent decrease in microvascular complications among patients who had intensive blood sugar control.
The DCCT findings corroborate results of the United Kingdom Prospective Diabetes Study (UKPDS), which concluded that every percentage point drop in HbA1c meant a 35-percent reduction in the risk of microvascular complications. The DCCT and UKPDS data clearly showed that good blood glucose control translate clinically into sight preservation.
Another common ophthalmologic complication in diabetic patients is the formation of premature cataracts. Despite similarities with senile cataracts in presentation and nature, premature cataracts in diabetics present at a younger age and are associated to the duration of diabetes and the severity of chronic hyperglycemia. Nonenzymatic glycolysation of the lens protein induces cataract formation in humans. This process, however, is faster among diabetics because high blood sugar levels account for faster non-enzymatic glycosylation of the lens protein.