By Paul Walia, M.D. of Georgia Retina
Diabetic retinopathy affects nearly one-third of all patients with diabetes and is the leading cause of visual impairment and blindness in working-aged adults. The Centers for Disease Prevention and Control (CDC) estimates that currently the healthcare costs associated with the treatment for diabetic retinopathy is around $500 million annually. Projections forecast that from 2010 to 2050, the number of Americans with diabetic retinopathy is expected to nearly double, from 7.7 million to 14.6 million, mirroring trends with obesity and metabolic syndrome.
Diabetic retinopathy often begins without symptoms. It invariably affects both eyes and is usually symmetric. If asymmetric disease is present with one eye having severe changes and the other eye not showing manifestation, the ophthalmologist must be alerted to unilateral hypoperfusion, specifically carotid artery insufficiency or blockage.
Patients may have relatively good and even perfect vision at initial presentation. However as the disease progresses, patients may experience distortion of vision, floaters and decrease of vision from mild diminution to total loss of vision.
The pathophysiology of diabetic retinopathy is complex. Hyperglycemia induces vascular pericyte deficiency, which leads to an increased vascular permeability and leakage and release of pro-inflammatory cytokines. This leads to local ischemia. Clinically, increased vascular permeability is most evident as microaneurysms, cotton-wool spots, intraretinal hemorrhages, the presence of exudates and macular edema. Ischemia is discernible as the presence of neovascularization.
The two sight-threatening consequences are diabetic macular edema and proliferative diabetic retinopathy. Diabetic macular edema (Figure 1) affects the macula, and thus the central vision is reduced. Focal laser treatment to photocoagulate the leaking microaneurysms has long been proven an effective therapy. Advances in pharmacotherapy have allowed intravitreal injections of medication to revolutionize the treatment paradigm. (See Figure 2.)
Medications such as anti-VEGF monoclonal antibodies and corticosteroids are vital tools in the retina specialists’ tool chest to treat diabetic macular edema. A challenge with these medications, however, is that they require multiple and ongoing injections at various intervals based on their pharmacokinetics. Promising research is ongoing about other drug-delivery vehicles, such as implantable biodegradable implants, that can allow sustained delivery of medication and reduce the frequency of injections. Additionally, there are several oral medications being studied that in conjunction with intravitreal injections may reduce the treatment burden.
Proliferative diabetic retinopathy is marked by the presence of neovascularization. (See Figure 3.) The new compensatory vessels that develop in response to ischemia lack structural integrity. They can burst and result in massive vitreous hemorrhage or fibrose and cause traction retinal detachments. Treatment options include intravitreal injection, pan-retinal laser photocoagulation of ischemic retina and vitrectomy to remove vitreous hemorrhages and delaminate the tractional tissue from the retinal surface. Improvements in vitreoretinal surgery, including small-gauge incisions, improving viewing systems and enhancements to microsurgical instruments, have allowed retina surgeons to achieve superior outcomes.
While specialists who care for retinal diseases have a variety of treatment options to address diabetic retinopathy, prevention remains crucial. Early detection is essential to reducing the devastating consequences that can occur. Estimates suggest that a routine comprehensive dilated eye exam at least once a year can reduce the risk of eye disease by 54 percent to 76 percent and lead to the early detection of eye disease.
Of paramount importance in the treatment of diabetic retinopathy is the optimization of hyperglycemia. According to The Diabetes Control and Complications Trial, controlling diabetes and maintaining the HbA1c level in the 6 percent to 7 percent range can delay the onset or substantially reduce the progression of diabetic retinopathy. Additional risk factors for progression of diabetic retinopathy include male sex, longer duration of diabetes, insulin use and higher systolic blood pressure as well as African-American or Hispanic ethnicity.
As the number of patients with diabetes escalates, all physicians taking care of diabetic patients will be faced with the challenge of managing this chronic disease. With early detection, systemic control and retinal therapeutics, ophthalmologists who focus on retinal care are prepared to handle the fight against diabetic retinopathy.
Note- Figures 1 and 3 are courtesy of the Wills Eye Manual.
Saaddine JB, Honeycutt AA, Narayan KM, et al. Projection of diabetic retinopathy and other major eye diseases among people with diabetes mellitus: United States, 2005–2050. Arch Ophthalmol 2008;126(12):1740–1747.
The Wills Eye Manual : Office and Emergency Room Diagnosis and Treatment of Eye Disease. Sixth Edition. Philadelphia :Lippincott, Williams, and Wilkins. 2012.
King P, Peacock I, Donnelly R. The UK Prospective Diabetes Study (UKPDS): clinical and therapeutic implications for Type 2 Diabetes. Br J Clin Pharmacol. 1999. 48: 643-8.
Nathan D. The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Study at 30 Years: Overview. Diabetes Care. 2014. 37: 9-16