Signs and Symptoms
Diabetes mellitus is the most common endocrine disorder, and is defined as a group of disorders that exhibit a defective or deficient insulin secretory process, glucose underutilization, and hyperglycemia. Possible systemic signs and symptoms include polyuria (increased frequency of urination), polydipsia (increased thirst), polyphagia (increased appetite), glycosuria, weakness, weight loss, neuropathy, and nephropathy. Ophthalmic signs and symptoms may include chronic conjunctival injection, changes in corneal curvature, large fluctuations in refraction, premature cataractogenesis, nonproliferative and proliferative retinopathy and cranial nerve III, IV or VI palsy.
Type 1 diabetes, formerly known as insulin-dependent diabetes (IDDM) is also referred to as juvenile-onset or ketose prone DM, usually begins by age 20 and is defined by a severe, absolute lack of insulin caused by a reduction in the beta-cell mass of the pancreas. This may be the result of autoimmune processes and may involve genetic susceptibility.
Type 2 diabetes, formerly known as non-insulin-dependent diabetes (NIDDM), sometimes referred to as adult-onset DM, usually begins after age 40 as a multifactorial disease that may involve improper insulin secretion, malfunctioning insulin and/or insulin resistance in peripheral tissues. Approximately 10 percent of diabetic cases are type 1 and approximately 90 percent are Type 2.
The pancreas plays a primary role in the metabolism of glucose by secreting the hormones insulin and glucagon. The Islets of Langerhans secrete insulin and glucagon directly into the blood. Inadequate secretion of insulin, inadequate structure or function of insulin or its receptors results in impaired metabolism of glucose, carbohydrates, proteins and fats, characterized by hyperglycemia and glycosuria. Hyperglycemia is the most frequently observed sign of diabetes and is considered the etiologic source of diabetic complications both in the body and in the eye.
Glucagon is a hormone that opposes the action of insulin. It is secreted when blood glucose levels fall. Glucagon increases blood glucose concentration partly by breaking down glycogen in the liver. Following a meal, glucose is absorbed into the blood. In response to increased blood glucose levels, insulin is secreted causing rapid uptake, storage, or use of glucose by the tissues of the body. Unused glucose is stored as glycogen in the liver. Between meals, when blood glucose is at minimal levels, tissues continue to require an energy source to function properly. Stored glycogen, via glucagon, is converted to glucose by a pathway known as glycogenolysis. Gluconeogenesis is the production of glucose in the liver from noncarbohydrate precursors such as glycogenic amino acids.
Elevated glucose levels result in the formation of sorbitol (a sugar alcohol) via the aldose reductase pathway. Since sorbitol cannot readily diffuse through cell membranes, cell edema and changes in function can ensue. With respect to the eye, this contributes to the evolution of premature cataractogenesis (nuclear sclerotic, senile and snowflake posterior subcapsular cataracts) and sight threatening diabetic retinopathy (compromising the pericytes that line capillary walls).
An additional complication of hyperglycemia is nonenzymatic glycosylation. Nonenzymatic glycosylation is the binding of excess glucose to the amino group of proteins in the tissues. As a possible result, at the level of the capillary membranes, altered cell function may lead to the development of microaneurysms, vascular loops, and vessel dilation, allowing blood leakage. Platelet aggregation secondary to these changes initiates tissue hypoxia. These changes result in the system wide accumulation of edema and in the eye, increase the potential for retinal sequelae.
Glycemic control over the course of the disease has been shown to reduce the risk of developing debilitating organ disease and retinopathy. Blood glucose levels are of even greater importance in diabetic pregnant women, as hyperglycemia during pregnancy may initiate swift and severe progression of diabetic retinopathy. Other concurrent systemic variables that may potentiate the onset of diabetic retinopathy include hypertension, nephropathy, cardiac disease, autonomic neuropathy and ocular findings such as elevated intraocular pressure and myopia.
The easiest method of treating Type 2 diabetes is with diet control. Dietary regulation is set by basing the caloric intake on the patient’s ideal body weight, selecting adequate sources of protein and carbohydrate, while maintaining a reasonable distribution of foods. When hyperglycemia persists despite dietary changes, oral hypoglycemic agents become necessary. These agents can be prescribed in small doses, adjusting the dosage to larger levels to achieve tighter control, as necessary.
Insulin is always required for Type 1 and is an option for recalcitrant cases involving Type 2 diabetes. Conventional therapy involves the administration of an intermediate-acting insulin (NPH or lente), once or twice a day, with or without small amounts of regular insulin.
Large changes in refraction may be the first sign of diabetic disease. Often, myopic or hyperopic shifts are created as the lens swells, secondary to sorbitol effects, resulting in large refractive changes, in what were otherwise noted as "stable eyes."