Patients with diabetes often develop ophthalmic complications, such as corneal abnormalities, glaucoma, iris neovascularization, cataracts, and neuropathies. The most common and potentially most blinding of these complications, however, is diabetic retinopathy,
which is, in fact, the leading cause of new blindness in persons aged 25-74 years in the United States. Approximately 700,000 persons in the United States have proliferative diabetic retinopathy, with an annual incidence of 65,000. An estimate of the prevalence of diabetic retinopathy in the United States showed a high prevalence of 28.5% among those with diabetes aged 40 years or older.
Diabetes mellitus (DM) is a major medical problem throughout the world. Diabetes causes an array of long-term systemic complications that have considerable impact on the patient as well as society, as the disease typically affects individuals in their most productive years.
An increasing prevalence of diabetes is occurring throughout the world.
In addition, this increase appears to be greater in developing countries. The etiology of this increase involves changes in diet, with higher fat intake, sedentary lifestyle changes, and decreased physical activity.
Important aspects of workup regarding diabetic retinopathy include fasting glucose and hemoglobin A1c (HbA1c), fluorescein angiography, optical coherence tomography, and B-scan ultrasonography. Controlling diabetes and maintaining the HbA1c level in the 6-7% range are the goals in the optimal management of diabetes and diabetic retinopathy.
The exact mechanism by which diabetes causes retinopathy remains unclear, but several theories have been postulated to explain the typical course and history of the disease.
See the image below.
Fundus photograph of early background diabetic retinopathy showing multiple microaneurysms.
In the initial stages of diabetic retinopathy, patients are generally asymptomatic, but in more advanced stages of the disease patients may experience symptoms that include floaters, distortion, and/or blurred vision. Microaneurysms are the earliest clinical sign of diabetic retinopathy. (See Clinical Presentation.)
Renal disease, as evidenced by proteinuria and elevated blood urea nitrogen (BUN)/creatinine levels, is an excellent predictor of retinopathy; both conditions are caused by DM-related microangiopathies, and the presence and severity of one reflects that of the other. Aggressive treatment of the nephropathy may slow progression of diabetic retinopathy and neovascular glaucoma. (See Treatment and Management.)
A study by Ito et al indicated that in patients with type 2 diabetes, the presence of reduced peripheral nerve conduction velocity is associated with the existence of early diabetic retinopathy. The report included 42 patients with type 2 diabetes (42 eyes), who had either no diabetic retinopathy or mild nonproliferative diabetic retinopathy. The investigators found that the latter group had significantly lower sural sensory conduction velocity and tibial motor conduction velocity than did patients with no diabetic retinopathy, with logistic regression analysis showing these velocities to be independent risk factors for the mild nonproliferative eye disease.
According to The Diabetes Control and Complications Trial controlling diabetes and maintaining the HbA1c level in the 6-7% range can substantially reduce the progression of diabetic retinopathy. (See Treatment and Management.)
One of the most important aspects in the management of diabetic retinopathy is patient education. Inform patients that they play an integral role in their own eye care. (See Patient Education.)
For more information, see Type 1 Diabetes Mellitus and Type 2 Diabetes Mellitus.
Signs and symptoms of diabetic retinopathy
In the initial stages of diabetic retinopathy, patients are generally asymptomatic; in the more advanced stages of the disease, however, patients may experience symptoms that include floaters, blurred vision, distortion, and progressive visual acuity loss. Signs of diabetic retinopathy include the following:
Microaneurysms: The earliest clinical sign of diabetic retinopathy; these occur secondary to capillary wall outpouching due to pericyte loss; they appear as small, red dots in the superficial retinal layers
Dot and blot hemorrhages: Appear similar to microaneurysms if they are small; they occur as microaneurysms rupture in the deeper layers of the retina, such as the inner nuclear and outer plexiform layers
Flame-shaped hemorrhages: Splinter hemorrhages that occur in the more superficial nerve fiber layer
Retinal edema and hard exudates: Caused by the breakdown of the blood-retina barrier, allowing leakage of serum proteins, lipids, and protein from the vessels
Cotton-wool spots: Nerve fiber layer infarctions from occlusion of precapillary arterioles; they are frequently bordered by microaneurysms and vascular hyperpermeability
Venous loops and venous beading: Frequently occur adjacent to areas of nonperfusion; they reflect increasing retinal ischemia, and their occurrence is the most significant predictor of progression to proliferative diabetic retinopathy (PDR).
Intraretinal microvascular abnormalities: Remodeled capillary beds without proliferative changes; can usually be found on the borders of the nonperfused retina
Macular edema: Leading cause of visual impairment in patients with diabetes
Nonproliferative diabetic retinopathy
Mild: Indicated by the presence of at least 1 microaneurysm
Moderate: Includes the presence of hemorrhages, microaneurysms, and hard exudates
Severe (4-2-1): Characterized by hemorrhages and microaneurysms in 4 quadrants, with venous beading in at least 2 quadrants and intraretinal microvascular abnormalities in at least 1 quadrant
Proliferative diabetic retinopathy
Neovascularization: Hallmark of PDR
Preretinal hemorrhages: Appear as pockets of blood within the potential space between the retina and the posterior hyaloid face; as blood pools within this space, the hemorrhages may appear boat shaped
Hemorrhage into the vitreous: May appear as a diffuse haze or as clumps of blood clots within the gel
Fibrovascular tissue proliferation: Usually seen associated with the neovascular complex; may appear avascular when the vessels have already regressed
Traction retinal detachments: Usually appear tented up, immobile, and concave
See Clinical Presentation for more detail.
Diagnosis of diabetic retinopathy
Laboratory studies of HbA1c levels are important in the long-term follow-up care of patients with diabetes and diabetic retinopathy.
Imaging studies used in the diagnosis of diabetic retinopathy include the following:
Fluorescein angiography: Microaneurysms appear as pinpoint, hyperfluorescent lesions in early phases of the angiogram and typically leak in the later phases of the test
Optical coherence tomography scanning: Administered to determine the thickness of the retina and the presence of swelling within the retina, as well as vitreomacular traction
See Workup for more detail.
Management of diabetic retinopathy
This includes the following:
Triamcinolone: Administered intravitreally; corticosteroid used in the treatment of diabetic macular edema
Bevacizumab: Administered intravitreally; monoclonal antibody that can help to reduce diabetic macular edema and neovascularization of the disc or retina
Ranibizumab: Administered intravitreally; monoclonal antibody that can help to reduce diabetic macular edema and neovascularization of the disc or retina
The Diabetes Control and Complications Trial found that intensive glucose control in patients with type 1 diabetes (previously called insulin-dependent diabetes mellitus [IDDM]) decreased the incidence and progression of diabetic retinopathy.
It may be logical to assume that the same principles apply in type 2 diabetes (previously called non-insulin-dependent diabetes mellitus [NIDDM]).
This involves directing a high-focused beam of light energy to create a coagulative response in the target tissue. In nonproliferative diabetic retinopathy (NPDR), laser photocoagulation is indicated in the treatment of clinically significant macular edema.
Panretinal photocoagulation (PRP) is used in the treatment of PDR.
It involves applying laser burns over the entire retina, sparing the central macular area.
This procedure can be used in PDR in cases of long-standing vitreous hemorrhage (where visualization of the status of the posterior pole is too difficult), tractional retinal detachment, and combined tractional and rhegmatogenous retinal detachment.
When laser photocoagulation in PDR is precluded in the presence of an opaque media, such as in cases of cataracts or vitreous hemorrhage, cryotherapy may be applied instead.
See Treatment and Medication for more detail.