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Diabetic Retinopathy

  • Author: Abdhish R Bhavsar, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Mar 31, 2015
 

Practice Essentials

Diabetic retinopathy is the leading cause of new blindness in persons aged 25-74 years in the United States. 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.[1, 2] See the image below.

Fundus photograph of early background diabetic ret Fundus photograph of early background diabetic retinopathy showing multiple microaneurysms.

Signs and symptoms

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
  • Macular edema

See Clinical Presentation for more detail.

Diagnosis

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
  • B-scan ultrasonography

See Workup for more detail.

Management

Pharmacologic therapy

  • 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

Glucose control

The Diabetes Control and Complications Trial found that intensive glucose control in patients with insulin-dependent diabetes mellitus (IDDM) decreased the incidence and progression of diabetic retinopathy.[3, 4, 5] It may be logical to assume that the same principles apply in non-insulin-dependent diabetes mellitus (NIDDM).

Laser photocoagulation

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.[6, 7] It involves applying laser burns over the entire retina, sparing the central macular area.

Vitrectomy

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.

Cryotherapy

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.

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Background

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.[8] An increasing prevalence of diabetes is occurring throughout the world.[9] 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.[10, 11]

Diabetic retinopathy is 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. A recent 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 and older.[12] (See Epidemiology.)

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.[13, 14]

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 and blurred vision. Microaneurysms are the earliest clinical sign of diabetic retinopathy. (See Clinical Presentation.)

Workup for diabetic retinopathy includes fasting glucose and hemoglobin A1c measurements. (See Workup.)

Renal disease, as evidenced by proteinuria and elevated 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.)

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.

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Pathophysiology

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.[1, 2]

Fundus photograph of early background diabetic ret Fundus photograph of early background diabetic retinopathy showing multiple microaneurysms.

Growth hormone

Growth hormone appears to play a causative role in the development and progression of diabetic retinopathy. Diabetic retinopathy has been shown to be reversible in women who had postpartum hemorrhagic necrosis of the pituitary gland (Sheehan syndrome). This led to the controversial practice of pituitary ablation to treat or prevent diabetic retinopathy in the 1950s. This technique has since been abandoned because of numerous systemic complications and the discovery of the effectiveness of laser treatment.

Platelets and blood viscosity

The variety of hematologic abnormalities seen in diabetes, such as increased erythrocyte aggregation, decreased red blood cell deformability, increased platelet aggregation, and adhesion, predispose the patient to sluggish circulation, endothelial damage, and focal capillary occlusion. This leads to retinal ischemia, which, in turn, contributes to the development of diabetic retinopathy.

Aldose reductase and vasoproliferative factors

Fundamentally, diabetes mellitus (DM) causes abnormal glucose metabolism as a result of decreased levels or activity of insulin. Increased levels of blood glucose are thought to have a structural and physiologic effect on retinal capillaries causing them to be both functionally and anatomically incompetent.

A persistent increase in blood glucose levels shunts excess glucose into the aldose reductase pathway in certain tissues, which converts sugars into alcohol (eg, glucose into sorbitol, galactose to dulcitol). Intramural pericytes of retinal capillaries seem to be affected by this increased level of sorbitol, eventually leading to the loss of their primary function (ie, autoregulation of retinal capillaries). This results in weakness and eventual saccular outpouching of capillary walls. These microaneurysms are the earliest detectable signs of DM retinopathy. (See the image below.)

Fundus photograph of early background diabetic ret Fundus photograph of early background diabetic retinopathy showing multiple microaneurysms.

Using nailfold video capillaroscopy, a high prevalence of capillary changes is detected in patients with diabetes, particularly those with retinal damage. This reflects a generalized microvessel involvement in both type 1 and type 2 diabetes.[15]

Ruptured microaneurysms result in retinal hemorrhages either superficially (flame-shaped hemorrhages) or in deeper layers of the retina (blot and dot hemorrhages). (See the image below.)

Retinal findings in background diabetic retinopath Retinal findings in background diabetic retinopathy, including blot hemorrhages (long arrow), microaneurysms (short arrow), and hard exudates (arrowhead).

Increased permeability of these vessels results in leakage of fluid and proteinaceous material, which clinically appears as retinal thickening and exudates. If the swelling and exudation involve the macula, a diminution in central vision may be experienced.

Macular edema

Macular edema is the most common cause of vision loss in patients with nonproliferative diabetic retinopathy (NPDR). However, it is not exclusively seen in patients with NPDR; it may also complicate cases of proliferative diabetic retinopathy.

Fluorescein angiogram demonstrating foveal dye lea Fluorescein angiogram demonstrating foveal dye leakage caused by macular edema.
Fundus photograph of clinically significant macula Fundus photograph of clinically significant macular edema demonstrating retinal exudates within the fovea.

Another theory to explain the development of macular edema focuses on the increased levels of diacylglycerol from the shunting of excess glucose. This is thought to activate protein kinase C, which, in turn, affects retinal blood dynamics, especially permeability and flow, leading to fluid leakage and retinal thickening.

Hypoxia

As the disease progresses, eventual closure of the retinal capillaries occurs, leading to hypoxia. Infarction of the nerve fiber layer leads to the formation of cotton-wool spots, with associated stasis in axoplasmic flow.

More extensive retinal hypoxia triggers compensatory mechanisms in the eye to provide enough oxygen to tissues. Venous caliber abnormalities, such as venous beading, loops, and dilation, signify increasing hypoxia and almost always are seen bordering the areas of capillary nonperfusion. Intraretinal microvascular abnormalities represent either new vessel growth or remodeling of preexisting vessels through endothelial cell proliferation within the retinal tissues to act as shunts through areas of nonperfusion.

Neovascularization

Further increases in retinal ischemia trigger the production of vasoproliferative factors that stimulate new vessel formation. The extracellular matrix is broken down first by proteases, and new vessels arising mainly from the retinal venules penetrate the internal limiting membrane and form capillary networks between the inner surface of the retina and the posterior hyaloid face. (See the images below.)

New vessel formation on the surface of the retina New vessel formation on the surface of the retina (neovascularization elsewhere)
An area of neovascularization that leaks fluoresce An area of neovascularization that leaks fluorescein on angiography.
Boat-shaped preretinal hemorrhage associated with Boat-shaped preretinal hemorrhage associated with neovascularization elsewhere.

In patients with proliferative diabetic retinopathy (PDR), nocturnal intermittent hypoxia/reoxygenation that results from sleep-disordered breathing may be a risk factor for iris and/or angle neovascularization.[16]

Neovascularization is most commonly observed at the borders of perfused and nonperfused retina and most commonly occurs along the vascular arcades and at the optic nerve head. The new vessels break through and grow along the surface of the retina and into the scaffold of the posterior hyaloid face. By themselves, these vessels rarely cause visual compromise, but they are fragile and highly permeable. These delicate vessels are disrupted easily by vitreous traction, which leads to hemorrhage into the vitreous cavity or the preretinal space.

These new blood vessels initially are associated with a small amount of fibroglial tissue formation. However, as the density of the neovascular frond increases, so does the degree of fibrous tissue formation.

In later stages, the vessels may regress, leaving only networks of avascular fibrous tissue adherent to both the retina and the posterior hyaloid face. As the vitreous contracts, it may exert tractional forces on the retina via these fibroglial connections. Traction may cause retinal edema, retinal heterotropia, and both tractional retinal detachments and retinal tear formation with subsequent detachment.

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Etiology

Duration of diabetes

In patients with type I diabetes, no clinically significant retinopathy can be seen in the first 5 years after the initial diagnosis of diabetes is made. After 10-15 years, 25-50% of patients show some signs of retinopathy. This prevalence increases to 75-95% after 15 years and approaches 100% after 30 years of diabetes. Proliferative diabetic retinopathy (PDR) is rare within the first decade of type I diabetes diagnosis but increases to 14-17% by 15 years, rising steadily thereafter.

In patients with type II diabetes, the incidence of diabetic retinopathy increases with the disease duration. Of patients with type II diabetes, 23% have nonproliferative diabetic retinopathy (NPDR) after 11-13 years, 41% have NPDR after 14-16 years, and 60% have NPDR after 16 years.

Hypertension and hyperlipidemia

Systemic hypertension, in the setting of diabetic nephropathy, correlates well with the presence of retinopathy. Independently, hypertension also may complicate diabetes in that it may result in hypertensive retinal vascular changes superimposed on the preexisting diabetic retinopathy, further compromising retinal blood flow.

Proper management of hyperlipidemia (elevated serum lipids) may result in less retinal vessel leakage and hard exudate formation, but the reason behind this is unclear.

Pregnancy

Pregnant women with proliferative diabetic retinopathy do poorly without treatment, but those who have had prior panretinal photocoagulation remain stable throughout pregnancy. Pregnant women without diabetic retinopathy run a 10% risk of developing NPDR during their pregnancy; of those with preexisting NPDR, 4% progress to the proliferative type.

For more information, see Diabetes Mellitus and Pregnancy.

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Epidemiology

Of the approximately 16 million Americans with diabetes, 50% are unaware that they have it. Of those who know they have diabetes, only half receive appropriate eye care. Thus, it is not surprising that diabetic retinopathy is the leading cause of new blindness in persons aged 25-74 years in the United States.

Approximately 700,000 Americans have proliferative diabetic retinopathy, with an annual incidence of 65,000. Approximately 500,000 persons have clinically significant macular edema, with an annual incidence of 75,000.

Diabetes is responsible for approximately 8000 eyes becoming blinded each year, meaning that diabetes is responsible for 12% of blindness.[17] The rate is even higher among certain ethnic groups. An increased risk of diabetic retinopathy appears to exist in patients of Native American, Hispanic, and African American heritage.

With increasing duration of diabetes or with increasing age since its onset, there is a higher risk of developing diabetic retinopathy and its complications, including diabetic macular edema or proliferative diabetic retinopathy.

For more information, see Macular Edema.

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Prognosis

Prognostic factors that are favorable for visual loss include the following:

  • Circinate exudates of recent onset
  • Well-defined leakage
  • Good perifoveal perfusion

Prognostic factors that are unfavorable for visual loss include the following:

  • Diffuse edema/multiple leaks
  • Lipid deposition in the fovea
  • Macular ischemia
  • Cystoid macular edema
  • Preoperative vision of less than 20/200
  • Hypertension

Approximately 8,000 eyes become blind yearly because of diabetes. The treatment of diabetic retinopathy entails tremendous costs, but it has been estimated that this represents only one eighth of the costs of Social Security payments for vision loss. This cost does not compare to the cost in terms of loss of productivity and quality of life.

The Early Treatment for Diabetic Retinopathy Study has found that laser surgery for macular edema reduces the incidence of moderate visual loss (doubling of visual angle or roughly a 2-line visual loss) from 30% to 15% over a 3-year period. The Diabetic Retinopathy Study has found that adequate scatter laser panretinal photocoagulation reduces the risk of severe visual loss (< 5/200) by more than 50%.[18, 19]

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Patient Education

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.

Excellent glucose control is beneficial in any stage of diabetic retinopathy. It delays the onset and slows down the progression of the diabetic complications in the eye.

The following symptoms and/or health concerns must be addressed in any patient education program for those with diabetic retinopathy:

  • Systemic problems (eg, hypertension, renal disease, and hyperlipidemia) may contribute to disease progression.
  • Smoking, although not directly proven to affect the course of the retinopathy, may further compromise oxygen delivery to the retina. Therefore, all efforts should be made in the reduction, if not outright cessation, of smoking.
  • Visual symptoms (eg, vision changes, floaters, distortion, redness, pain) could be manifestations of disease progression and should be reported immediately.

Diabetes mellitus, in general, and diabetic retinopathy, in particular, are progressive conditions, and regular follow-up care with a physician is crucial for detection of any changes that may benefit from treatment.

For excellent patient education resources, see eMedicineHealth's Diabetes Center. Also, visit eMedicineHealth's patient education article Diabetic Eye Disease.

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Contributor Information and Disclosures
Author

Abdhish R Bhavsar, MD Adjunct Assistant Professor, Department of Ophthalmology, University of Minnesota Medical School; Director of Clinical Research, Retina Center, PA; Past Chair, Consulting Staff, Department of Ophthalmology, Phillips Eye Institute

Abdhish R Bhavsar, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Medical Association, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Minnesota Medical Association

Disclosure: Received grant/research funds from Allergan; Received grant/research funds from genentech; Received grant/research funds from regeneron; Received grant/research funds from sirion for none; Received consulting fee from Eyetech for consulting; Received consulting fee from Allergan for consulting; Received consulting fee from regeneron for consulting; Received travel reimbursement from Allergan for consulting.

Coauthor(s)

John H Drouilhet, MD, FACS Clinical Professor, Department of Surgery, Section of Ophthalmology, University of Hawaii, John A Burns School of Medicine

John H Drouilhet, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Medical Association

Disclosure: Nothing to disclose.

Neal H Atebara, MD Private Practice, Retina Center of Hawaii

Neal H Atebara, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Retina Society, American Medical Association, Hawaii Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

V Al Pakalnis, MD, PhD Professor of Ophthalmology, University of South Carolina School of Medicine; Chief of Ophthalmology, Dorn Veterans Affairs Medical Center

V Al Pakalnis, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, South Carolina Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Sherman O Valero, MD, to the development and writing of this article.

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Fundus photograph of early background diabetic retinopathy showing multiple microaneurysms.
Retinal findings in background diabetic retinopathy, including blot hemorrhages (long arrow), microaneurysms (short arrow), and hard exudates (arrowhead).
Fluorescein angiogram demonstrating an area of capillary nonperfusion (arrow).
Fluorescein angiogram demonstrating foveal dye leakage caused by macular edema.
Fundus photograph of clinically significant macular edema demonstrating retinal exudates within the fovea.
New vessel formation on the surface of the retina (neovascularization elsewhere)
An area of neovascularization that leaks fluorescein on angiography.
Boat-shaped preretinal hemorrhage associated with neovascularization elsewhere.
Fibrovascular proliferations within the vitreous cavity
Extensive fibrovascular proliferations within and around the optic disc
 
 
 
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