Article Date: 2/1/2007

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Screen for Diabetes
Play a role in the early detection of this devastating disease.

A total of 20.8 million people, or 7% of the U.S. population has some form of diabetes, according to the National Diabetes Information Clearing-house.1 Of these, 14.6 million have been diagnosed, while a total of 6.2 million people re-main undiagnosed.1 Further, about one in every 400 to 600 children and adolescents has Type-1 diabetes. Regional studies and clinically based reports propose that Type-2 diabetes is being diagnosed more often in chil- dren and adolescents, especially in those of Native American, Af-rican American and Hispan-ic/Latino American descent.1 Also, diabetes is the leading cause of new cases of blindness among adults ages 20 to 74, and diabetic retinopathy causes 12,000 to 24,000 new cases of blindness each year.1

Although you are no doubt aware of the clinical signs and symptoms of diabetic retinopathy, you should also be aware of the clinical signs and symptoms of this entire disease, as patients may be more likely to see you than their primary-care practitioner on a regular basis (see "Essentials of Diabetic Retinopathy," page 31). This means you play a vital role in the early detection of this disease and in the preservation of these patients' quality of life.

Here, I will provide an over-view of diabetes and how you can screen your patients for this disease, so you can refer them to their primary-care physicians for a definitive diagnosis in a timely fashion.

Diabetes overview

Diabetes is "a group of meta-bolic diseases characterized by hyperglycemia (an abnormally high level of glucose in the blood), resulting from defects in insulin secretion, insulin action or both."2 Insulin is a polypeptide hormone, produced by the beta cells of the islets of Langerhans of the pancreas. It regulates the metabolism of glucose (which provides the body with energy) as well as other nutrients. Glucagon, a hormone also secreted by the pancreas, opposes the effects of insulin. These two hormones work together to maintain a homeostatic mechanism for blood glucose levels. Insulin enters the blood stream shortly after a person eats, particularly those food items rich in carbohydrates. When the body needs glucose, insulin facilitates its use to meet the body's needs. Any excess glucose converts to glycogen, which is stored in the liver or muscle or as fatty tissue.

Glucagon is secreted during the fasting states of the body by the alpha cells of the Islet of Langerhans. Glucagon elevates blood glucose levels by one of three mechanisms:
1. Glycogenolysis: breakdown of stored glycogen in the liver to make glucose.
2. Gluconeogenesis: conversion of non-glucose substrates into glucose.
3. Glucose sparing: a process in which ketones are formed in the liver. (Ketones are substanc-es made if your diet doesn't contain enough carbohydrates to supply the body with sugar [glucose] for energy or if your body can't use blood sugar [glucose] properly.)

Diabetes falls into one of two categories: Type-1 and Type-2:

Type-1 accounts for approximately 10% of all diabetes cases. Patients with Type-1 diabetes are typically young, thin and under-go a progressive loss of endogenous insulin leading to hypergly- cemia. The peak incidence of Type-1 diabetes: between ten and 13 years of age. In fact, 95% of patients who have Type-1 diabetes are diagnosed before age 25.3 This form of the disease is characterized by an autoimmune process, which causes beta cell destruction, usually leading to absolute insulin deficiency.

Type-2 diabetes accounts for more than 90% of the total disease population. Type-2 diabetes typically occurs in people who are older than age 40, are obese and/or have a family history of diabetes.

This form of the disease involves two major pathogenetic mechanisms: impaired islet-cell function (impaired insulin secretion) and impaired insulin action (insulin resistance or decreased insulin sensitivity). Insulin resistance occurs when normal concentrations of insulin elicit a less- than-normal biologic response. When this patient eats, some insulin secretion still occurs, but at reduced levels. Thus, the body cannot absorb and utilize all the glucose.

Patients who have Type-2 diabetes usually aren't dependent on insulin to maintain their life or prevent ketosis (when the body burns its own fat for fuel), but insulin is commonly necessary for them to maintain reasonable blood glucose concentrations.

Ultimately, diabetes alters the body's ability to metabolize carbohydrates. Chronic hypergly-cemia results in fats and proteins causing widespread damage throughout the body. This elevated blood sugar eventually causes damage to the kidneys, nerves, heart and blood vessels and the eyes in the form of ne-phropathy, neuropathy and leaky blood vessels.

The chronic complications of diabetes include organ-specific degenerative processes, such as accelerated vascular disease and neurologic deficits. The vascular disease consists of both microangiopathy and macroangiopathy. The former is a disease of the capillaries specifically associated with diabetes. It's characterized by thickening of capillary basement membranes and manifests clinically mostly in the retina and kidney. The latter is an accelerated form of atherosclerotic disease of the arteries that usually manifests clinically in the coronary arteries, cerebral arteries and peripheral vessels of the low-er extremities.

Screening for diabetes

To screen your patients for diabetes, include the following eight questions on your patient history form:

1. Do you have a first-degree relative (sibling, parent, child) who has diabetes? If the patient answers "yes," this means he is genetically predisposed to developing the disease.
2. Have you recently given birth to a baby weighing more 9 lbs? If the patient answers "yes," this means she is at high risk for diabetes because women with elevated blood sugar tend to have large babies.
3. Were you diagnosed with gestational diabetes during your pregnancy? If the patient an-swers "yes," this is important because women who've suffered from gestational diabetes are more likely to develop diabetes later in life.
4. Do you have hypertension? If the patient answers "yes," this is important, as patients who have hypertension are at higher risk for developing diabetes.
5. Do you have high cholesterol? If the patient answers "yes," this is significant, as a high-density lipoprotein level of 35mg per (deciLiter) dL (0.90mmol per L) or lower and/or a triglyceride level of 250mg per dL (2.83mmol per L) or higher puts a person at great risk for diabetes.
6. Have you been experiencing an increase in thirst (polydipsia)?
7. Have you been experiencing an increase in appetite (polyphagia)?
8. Have you been urinating more frequently (polyuria)?

"Yes" answers to questions six through eight indicate the classic triad symptoms of Type-1 diabetes. These patients are prone to ketoacidosis, a life-threatening complication caused by severe insulin deficiency, which can cause diabetic coma and death.4

Unlike Type-1 diabetes, in which the symptoms are pro-nounced, the onset of Type-2 diabetes is gradual. Therefore, primary-care physicians often diagnose Type-2 diabetes in asymptomatic patients during routine physical examinations when these patients' blood work shows elevated blood glucose levels.

If a patient older than age 45 presents for his annual exam, make screening for diabetes a yearly routine. This is because younger patients are less likely to develop adult-onset diabetes. If the patient's answers to the screening questions indicate he isn't a suspect for diabetes, repeat this screening at three-year intervals, as this is standard protocol.

If however, this patient or any other patient answers "yes" to any of the history questions, consider referring him or her to a primary-care physician for diagnostic testing for diabetes.

Because patients may be more likely to see you than their primary-care practitioner on a regular basis, you have the oppor- tunity to detect diabetes in these patients early by educating yourself on all the clinical signs and symptoms of this disease, passing this information to your patients, and including the necessary questions in your patient history form. Remember: Learning all you can about the systemic diseases that have ocular manifestations makes you a true pri- mary-care optometrist that patients will seek.

1. National Diabetes Information Clearinghouse (NDIC). National Diabetes Statistics. http://diabetes.niddk.nih. gov/dm/pubs/statistics/ (Accessed January 9, 2007).
2. The expert committee on the diagnosis and classification of diabetes mellitus. Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care 2003 Jan;26 (Supp 1):s5-20.
3. Saydah SH, Loria CM, Eberhardt MS, Brancati FL. Subclinical states of glucose intolerance and risk of death in


Diabetic retinopathy is the result of chronic elevation of blood glucose levels. It's usually more common in patients with uncon-trolled diabetes or those who have long-standing diabetes.

The production of "free radical" reactive oxygen species by the mitochondria generates several harmful biochemicals, such as vascular endothelial factor (VEGF), protein kinase C (PKC) and advanced glycosalated end products. The end result: damage to the integrity of retinal capillaries, causing them to become leaky.

The hallmark signs of diabetic retinopathy include microaneurysms, dot-and-blot intraretinal hemorrhages and hard exudates. Many patients also demonstrate cotton-wool spots, intraretinal micro-vascular abnormalities (IRMA), neovascularization of the disc (NVD), neovascularization elsewhere (NVE) and diabetic macular edema.

The classification of diabetic retinopathy has historically been based on the Early Treatment Diabetic Retinopathy Study (ETDRS), in which diabetic retinopathy was classified into "no diabetic retinopathy," "background retinopathy," "pre-proliferative and proliferative." the International Clinical Diabetic Retinopathy Disease Severity Scale is the newer classification (visit html).

Proper management of diabetic retinopathy is heavily dependent on the stage of the disease. So, it ranges from regular monitoring to photo-documentation to laser intervention. Your underlying management is to prevent or minimize diabetic retinopathy in all diabetic patients via sufficient control of blood glucose levels and proper control of blood pressure and blood lipids.

Optometric Management, Issue: February 2007