The Optometrist's Role in Diabetes
The Optometrist's Role in Diabetes
BY RAYMOND CHEW, O.D., Manchester, N.H.
Diabetes mellitus (DM) is a "group of diseases marked by high levels of blood glucose resulting from defects in insulin production, insulin action or both," according to the American Diabetes Association. The Centers for Disease Control (CDC) estimates 171 million people suffer from diabetes worldwide, with 20.8 million in the United States alone. These numbers will increase dramatically in the next 50 years.1 The care of DM and its related complications cost the United States $132 billion in 2002.2
Optometrists are the sole eye-care providers for 60% of communities in the United States, according to the American Optometric Association (AOA). This places us in a position to detect early signs of diabetic complications and to reduce the risk of vision loss through timely and appropriate referrals. Here's a brief review of DM and diabetic eye disease, so you can be in the position to help these patients.
Types of diabetes mellitus
The three major types of DM are:
• Type-1 DM. This type accounts for 5% to 10% of the diabetic population in the United States, according to the American Diabetes Association (ADA). It is caused by autoimmune destruction of the pancreatic cells, resulting in absolute insulin deficiency. These patients must receive insulin treatments to survive. The risk factors of type-1 DM are thought to be genetic, autoimmune and/or environmental. Type-1 DM may present with unexplained weight loss, polyuria, polyphagia or polydipsia.3
• Type-2 DM. The ADA reports this type accounts for 90% to 95% of the diabetic population in the United States and results from a combination of insulin resistance and insulin deficiency. Practitioners can generally treat type-2 DM with a combination of lifestyle modifications, oral medications and/or insulin therapy or other injectables. Patients with type-2 DM are often asymptomatic, but may also present with the same symptoms as type-1 DM patients or with blurred vision, impaired wound healing, recurrent infections or peripheral neuropathy.
Because type-2 DM is often not diagnosed until complications develop, the ADA recommends screening high-risk, asymptomatic individuals for DM and pre-diabetes. High-risk patients include those older than age 45, especially those who are overweight (body-mass index >25 kg/m2).
The ADA recommends retesting in three years if the patient's Fasting Plasma Glucose (FPG) or two-hour Oral Glucose Tolerance Test (two-hour OGTT) is normal. If the patient is younger or overweight and has additional risk factors for type-2 DM, he should be retested more frequently based on the patient's individual risk factors.3 (See "Risk Factors for Type-2 Diabetes Mellitus," below.)
• Gestational diabetes (GDM). Approximately 4% of pregnant women in the United States will develop GDM, according to ADA statistics. Treatment is required to prevent complications to the fetus. Those with GDM have an increased risk of developing type-2 DM, ranging up to a 70% risk in their lifetime. The patient's primary-care physician should screen her six- to 12 weeks post-partum. After pregnancy, patients have a 20% to 50% risk of developing diabetes in five to 10 years.3
The diagnosis of diabetes is based on the symptoms previously discussed and a casual plasma glucose >/= 200mg/dl, a FPG >/= 126mg/dl or a two-hour OGTT of >/= 200 mg/dl.
The potential complications of DM are:
• Cardiovascular and cerebrovascular disease. The ADA reports diabetes is a leading cause of death in the United States, and the life expectancy of a diabetic person is five to 10 years shorter than a person without DM. A major cause of death in diabetics is cardiovascular disease.4
The United Kingdom Prospective Diabetes Study (UKPDS) found that tight blood pressure (BP) control (treated with atenolol or captopril, along with a target BP of <150/85mm Hg) reduced the risk of diabetes-related deaths by 32%, myocardial infarction (MI) by 21%, cerebrovascular accident (CVA) by 44% and heart failure by 56%.5–6 The UKPDS also found that for every 1% reduction in hemoglobin A1C (Hgb A1C), there was a risk reduction of 14% for MI, 12% for CVA and 16% for heart failure.7 The ADA recommends a target blood pressure of >130/80mm Hg for all diabetics.
• Diabetic nephropathy. Diabetes is the leading cause of end-stage renal disease (ESRD).3 Diabetic nephropathy results in proteinuria, hypertension and progressive renal dysfunction.4 Microalbuminuria (creatinine 30–299g/mg) is an early sign of nephropathy. Intensive glycemic control, Angiotensin Converting Enzyme (ACE) inhibitors and Angiotensin Receptor Blockers (ARBs) have been shown to delay the progression of microalbuminuria to macroalbuminuria (creatinine >300g/mg).3
The UKPDS found that tight blood pressure control with either atenolol or captopril was associated with a reduction in risk of nephropathy and progression of renal failure.5–6 ESRD is the result of severe renal dysfunction, which ultimately requires chronic dialysis.
• Diabetic Retinopathy. Diabetes can have a detrimental effect on any portion of the visual system. Of the possible ophthalmic complications, diabetic retinopathy (DR) is the most visually destructive. CDC and ADA reports estimate that DR is the leading cause of new blindness in 20- to 74 year-olds in the U.S.
• Damage to several retinal cell types. DM results in damage to several retinal cell types, including neural cells, glial cells, pericytes and endothelial cells. Pericytes are responsible for maintaining endothelial cell function and growth. Endothelial cells normally function to maintain the blood-retina barrier. Pericyte damage results in endothelial cell dysfunction, altered vascular flow, vascular permeability and capillary perfusion.
Clinically, these changes manifest as intraretinal hemorrhages, microaneurysms, hard exudates, retinal edema, venous caliber abnormalities and intraretinal microvascular abnormalities. This process eventually leads to capillary closure and retinal ischemia, stimulating retinal neovascularization.
Recent studies have found various biochemical signals for the development of macular edema and neovascularization. Increased intraocular levels of vascular endothelial growth factor (VEGF) have been associated with neovascularization and increased vascular permeability.8–10
Further, hyperglycemia results in increased formation of advanced glycation end products (AGE), activation of the protein kinase C (PKC) pathway, increased activity of the aldose reductase pathway and increased oxidative stress, all of which contribute to diabetic retinopathy and macular edema.10,11
Another factor that may contribute to diabetic macular edema (DME): vitreomacular traction. It has been reported that practitioners can improve DME with either spontaneous or surgically induced posterior vitreous detachment.11
Diagnosis and management
The management of DR depends on the severity of retinopathy and the presence or absence of DME. When no DR or nonproliferative diabetic retinopathy (NPDR) exists, you can monitor the patient with dilated fundus examinations at appropriate time intervals (see "Recommended Follow-up and/or Treatment for Each Level of Retinopathy," above). When signs of proliferative diabetic retinopathy (PDR) and/or clinically significant macular edema (CSME) are present, you should refer the patient to a vitreoretinal specialist for timely and appropriate medical and/or surgical intervention.
• Risk factors. There are several modifiable systemic risk factors for diabetic retinopathy and macular edema: glycemic control, hypertension, dyslipidemia and smoking.12–14 Recent studies found only about 30% of patients with DM with known hypertension had adequately controlled blood pressure (<140/85mm Hg).15
The UKPDS and Diabetes Control and Complications Trial (DCCT) demonstrated the importance of optimal control of glycemia, and the UKPDS identified hypertension as an independent risk factor for progression of DR.5–7 For those with type-2 DM, the UKPDS found that intensive glycemic control (average Hgb A1C 7%) reduced microvascular complications (retinopathy and nephropathy) by 25%, and for every 1% reduction in hemoglobin A1C, the risks were reduced by 37%.7
The DCCT found that compared with conventional therapy (average Hgb A1C 9.1%), intensive therapy (average Hgb A1C 7.2%) reduced the incidence of severe NPDR (9% vs. 32%), neovascularization (8% vs. 24%) and CSME (9% vs. 27%) for those with type-1 DM.
The Early Treatment Diabetic Retinopathy Study (ETDRS) found that elevated total cholesterol (>240mg/dL), low-density lipoprotein (>160 mg/dL) and triglycerides (>399mg/dL) were associated with retinal hard exudates and reduced visual acuity. The ETDRS also found that 650mg of aspirin daily did not influence the frequency of vitreous or preretinal hemorrhages.
The ADA recommends a target Hgb A1C of less than 7% or as close to 6% without significant hypoglycemia, and a target blood pressure of <130/80mm Hg for all diabetics. The ADA further recommends reducing levels of LDL to <100mg/dL (<70mg/dL if the patient has heart disease) and TG <150mg/dL.
To treat clinically significant macular edema (CSME) and proliferative diabetic retinopathy (PDR):
• Refer the patient for laser photocoagulation. The Diabetes Retinopathy Study (DRS) was the first to evaluate the efficacy of scatter laser photocoagulation for the treatment of PDR. Early results showed a beneficial effect with PRP. Based on these two-year results, the recommendation was changed to perform scatter (panretinal) laser photocoagulation when patients have moderate or severe NVD or in the presence of vitreous or pre-retinal hemorrhage and mild NVD or at least 0.5mm disc area of NVE.
In the DRS, macular edema worsened after scatter laser photocoagulation. Later reports showed that focal laser or grid laser photocoagulation prior to scatter laser photocoagulation reduced a patient's risk of visual loss.
The ETDRS evaluated the timing of laser photocoagulation. The study found that early, full scatter treatment in eyes with at least moderate NPDR to mild PDR reduced the risk of progression to high-risk PDR by 50% compared with deferral until high-risk PDR developed. The ETDRS also found that focal laser photocoagulation for clinically significant macular edema (CSME) reduced risk of moderate vision loss (15 letters on ETDRS chart or three lines of acuity) by 50%. The ETDRS recommend prompt scatter laser for high-risk PDR and focal laser for CSME.
• Corticosteroids. Corticosteroids are a group of anti-inflammatory compounds that inhibit the VEGF gene. They are delivered as periocular or intravitreal injections, or implanted as sustained-release devices. While much of the literature is focused on triamcinolone acetonide, other corticosteroids have been used, including dexamethasone, fluocinolone acetonide and methylprednisolone acetate. Each treatment has been shown to improve vision and macular edema, as seen clinically.10,17,18
• VEGF inhibitors. VEGF is associated with neovascularization and increased vascular permeability. Pegaptanib (Macugen, Eyetech) and ranibizumab (Lucentis, Genentech) are currently FDA-approved treatments for exudative macular degeneration (wet-AMD). Pegaptanib is an aptamer that binds to the VEGF165 isoform of the VEGF-A gene. Ranibizumab is an antibody fragment that binds to all isoforms of the VEGF-A gene. A third VEGF inhibitor is bevacizumab (Avastin, Genentech). It is a full-length humanized monoclonal antibody that is FDA-approved for the treatment of certain colorectal cancers, but practitioners have also used it off-label for the treatment of wet AMD and macular edema.19 Phase-II studies have been performed or are ongoing for each of these VEGF inhibitors.16 Various studies have demonstrated each can improve visual acuity and reduce macular edema.
• Oral protein kinase-C inhibitors. PKC is another enzyme involved in neovascularization and increased vascular permeability. The Protein Kinase C — Diabetic Retinopathy Study (PKC-DRS) group studied Ruboxistaurin (RBX), an oral selective inhibitor of the PKC-B isoform. In 2005, the PKC-DRS group found that RBX did not have any effect on the progression of at least moderate to severe NPDR to PDR.20 Another study reported that RBX improved retinal vascular function in subjects without DR or with very mild NPDR without any serious adverse reactions.21 In 2006, the PKC-DRS2 group reported that RBX was associated with a reduction in sustained moderate vision loss (defined as a loss of 15 letters on two consecutive visits, six months apart) and a reduction in the progression of CSME with NPDR.22 (See, "Summary of Investigational Treatments," page 58.)
The O.D.'s role
You are positioned to be the primary eye-care provider for a significant portion of the population in the United States.
People with type-1 DM should have their first eye exam within three to five years of diagnosis, after the age of 10. People with type-2 DM should have their first eye exam at the time of diagnosis. Diabetics should have at least yearly, dilated fundus examinations. A diabetic medical history should include the type and duration of DM, past glycemic control, medications and systemic history. You should also inquire about the frequency and results of self-monitored blood glucose and recent laboratory tests for HgbA1C, serum lipids and proteinuria.
Perform gonioscopy when new vessels are visible on the iris. Be sure to clearly record the absence or presence and degree of signs of diabetic retinopathy. Document the degree of DR with drawings and/or other imaging devices. When you detect significant levels of DR, refer the patient for appropriate treatment.
It is important to take a few extra minutes to provide clear and concise patient education. You need to make patients aware of the need for timely eye care to reduce the risks of vision loss. You should also inform them of the importance of controlling systemic risk factors for the development and progression of DR and vision loss.
Many patients with DM are unaware of the association of hypertension and diabetes. Measuring blood pressure may be useful in identifying poorly controlled hypertension and in diagnosing new cases of hypertension.15 It also shows the patient that you feel it's important enough to take the time to measure his/her blood pressure.
In Australia, it was found that primary-care providers (PCPs) did not understand the level of care that optometrists can provide.23 This may also be true in the U.S. It's, therefore, also incumbent upon optometrists to communicate our findings to the patient's primary-care provider. OM
References furnished upon request.
||Dr. Chew graduated in 2002 from the New England College of Optometry in Boston. He has been Staff Optometrist at the Manchester Veterans Affairs Medical Center (VAMC) since 2003.|
Optometric Management, Issue: June 2007