Introduction
Background
Over the last several decades, there have been a few large-scale trials that have influenced the management of diabetic complications in the eye. Of these trials, only one, the Early Treatment Diabetic Retinopathy Study (ETDRS), identified macular edema as a study objective. To date, the ETDRS has presented the most comprehensive and detailed directives in the management of diabetic macular edema (DME). As a result, this article is based largely on the findings and conclusions of the ETDRS.
Pathophysiology
DME is the result of retinal microvascular changes that occur in patients with diabetes. Thickening of the basement membrane and reduction in the number of pericytes is believed to lead to increased permeability and incompetence of retinal vasculature. This compromise of blood-retinal barrier leads to the leakage of plasma constituents in the surrounding retina, resulting in retinal edema.
Frequency
United States
The World Health Organization (WHO) estimates that 15 million people have diabetes in the United States; one half of which are undiagnosed. Untreated, there is a 25-30% risk of developing clinically significant macular edema (CSME) with moderate visual loss.
International
The WHO estimates that more than 150 million people worldwide have diabetes.
Mortality/Morbidity
Diabetes is the leading cause of new blindness in the United States, to which CSME (see Physical for definition) has a significant contribution.
- Untreated, 25-30% of patients with CSME exhibit a doubling of the visual angle within 3 years.
- Treated, the risk drops by 50%.
Race
- Diabetes is more common in Latinos, African Americans, and Native Americans.
- No data describe the predilection of one racial group developing DME over another group.
Sex
No data describe the predilection of one sex developing DME over the other sex.
Age
Diabetic retinopathy (DR), not specifically DME, generally occurs in persons older than 40 years. It rarely occurs before puberty.
Clinical
History
- Ocular history
- Diabetic history - Specific inquiry should be made into risk factors for the development of DR.
- Type of diabetes - After 20 years of disease, nearly all patients with type I and 60% of patients with type II have some degree of retinopathy.
- Duration of the diabetes - Increased risk of DR
- Age of patient - DR is more likely to present in patients older than 40 years.
- Diabetic control - The Diabetes Control and Complication Trail (DCCT) has clearly demonstrated that tighter control of blood sugar is associated with reduced incidence of DR. (Glycosylated hemoglobin [HbA1c] should be less than 7%.)
- Renal disease - Proteinuria is a good marker for the development of DR; thus, patients with diabetic nephropathy should be observed more closely.
- Systemic hypertension - Increased risk of retinopathy (DR with superimposed hypertensive retinopathy)
- Triglycerides and lipids - Normalization of lipid levels reduces retinal leakage and exudates deposition.
- Pregnancy - DR can progress rapidly in pregnant women, especially those with preexisting DR.
Physical
Funduscopy under stereopsis and high magnification should be performed on every patient with diabetes to assess for DME and DR. An indirect ophthalmoscope does not provide adequate magnification for the ophthalmologist to diagnose DME.
- DME is defined as retinal thickening within 2 disc diameters of the center of the macula.
- Focal edema is associated with hard exudate rings resulting from leakage from microaneurysms.
- Diffuse edema results from breakdown of blood-retinal barrier with leakage from microaneurysms, retinal capillaries, and arterioles.
- CSME, as defined by the ETDRS, exists with any of the following findings:
- Retinal thickening within 500 µm of the center of the fovea
- Hard, yellow exudates within 500 µm of the center of the fovea with adjacent retinal thickening
- At least 1 disc area of retinal thickening, any part of which is within 1 disc diameter of the center of the fovea
- Other physical findings that should be noted include the following:
- Visual acuity is an important parameter in following the progression of CSME, although it does not aid in the diagnosis of CSME because patients may have a visual acuity of 20/20.
- The status of the posterior hyaloid; detached, taut, thickened
Causes
Causes include the following:
- After 20 years of the disease, nearly all patients with type I diabetes mellitus and 60% of patients with type II diabetes mellitus will have some degree of retinopathy.
- Poor control of blood sugar increases the risk of diabetic retinopathy.
- Renal disease can be a marker for the development of diabetic retinopathy.
- Systemic hypertension increases the risk of diabetic retinopathy.
- Elevated lipid levels increase the risk of leakage and exudate deposits.
More on Macular Edema, Diabetic |
Overview: Macular Edema, Diabetic |
| Differential Diagnoses & Workup: Macular Edema, Diabetic |
| Treatment & Medication: Macular Edema, Diabetic |
| Follow-up: Macular Edema, Diabetic |
| References |
| Next Page » |
References
Albert DM, Jakobiec FA. Principles and Practice of Ophthalmology. 2nd ed. Philadelphia: WB Saunders Co;2000.
Avitabile T, Longo A, Reibaldi A. Intravitreal triamcinolone compared with macular laser grid photocoagulation for the treatment of cystoid macular edema. Am J Ophthalmol. Oct 2005;140(4):695-702. [Medline].
Bonini-Filho MA, Jorge R, Barbosa JC, et al. Intravitreal injection versus sub-Tenon's infusion of triamcinolone acetonide for refractory diabetic macular edema: a randomized clinical trial. Invest Ophthalmol Vis Sci. Oct 2005;46(10):3845-9. [Medline].
Chew EY, Klein ML, Ferris FL 3rd, et al. Association of elevated serum lipid levels with retinal hard exudate in diabetic retinopathy. Early Treatment Diabetic Retinopathy Study (ETDRS) Report 22. Arch Ophthalmol. Sep 1996;114(9):1079-84. [Medline].
Cunningham ET, Adamis AP, Altaweel M, et al. A phase II randomized double-masked trial of pegaptanib, an anti-vascular endothelial growth factor aptamer, for diabetic macular edema. Ophthalmology. Oct 2005;112(10):1747-57. [Medline].
Fong DS, Segal PP, Myers F, et al. Subretinal fibrosis in diabetic macular edema. ETDRS report 23. Early Treatment Diabetic Retinopathy Study Research Group. Arch Ophthalmol. Jul 1997;115(7):873-7. [Medline].
Jonas JB, Martus P, Degenring RF, et al. Predictive factors for visual acuity after intravitreal triamcinolone treatment for diabetic macular edema. Arch Ophthalmol. Oct 2005;123(10):1338-43. [Medline].
Kertes. Clinical Trials in Ophthalmology: Summary and Practice Guide. Lippincott Williams & Wilkins;1998:15-35.
Otani T, Kishi S, Maruyama Y. Patterns of diabetic macular edema with optical coherence tomography. Am J Ophthalmol. Jun 1999;127(6):688-93. [Medline].
Patelli F, Fasolino G, Radice P, et al. Time course of changes in retinal thickness and visual acuity after intravitreal triamcinolone acetonide for diffuse diabetic macular edema with and without previous macular laser treatment. Retina. Oct-Nov 2005;25(7):840-5. [Medline].
Tachi N, Ogino N. Vitrectomy for diffuse macular edema in cases of diabetic retinopathy. Am J Ophthalmol. Aug 1996;122(2):258-60. [Medline].
Takagi H, Otani A, Kiryu J, Ogura Y. New surgical approach for removing massive foveal hard exudates in diabetic macular edema. Ophthalmology. Feb 1999;106(2):249-56; discussion 256-7. [Medline].
Further Reading
Keywords
diabetic macular edema, DME, diabetes, diabetic eye disease, diabetic eye complications, diabetic retinopathy, DR, retinal edema, macula
Overview: Macular Edema, Diabetic