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Managing patients with diabetic macular edema means focusing on a number of details to obtain a good clinical picture of each patient's status. These details include the location of the edema in the fovea, the nature of the evolution (acute, chronic, or progressive), status of the blood retinal barrier, signs of retinal pigment epithelial dysfunction, presence of retinal tissue damage, ischemia, vitreoretinal traction, status of metabolic control, and blood pressure.
Dr. Cunha-Vaz described the strategies he uses to manage DME in clinical practice at the Coimbra Centre of Vision Sciences and Ophthalmology, Coimbra, Portugal.
"When considering DME, we have to realize that sometimes ophthalmologists forget that the major issue is diabetes," he said.
"All of these factors are permanent in patients with diabetes," he said. "They play a role in DME. Ophthalmologists tend to focus on the eye, and these factors should not be overlooked."
Retinal endothelial cell injury is a major factor in diabetes. Two types of damage are included: the first is leakage in the inner blood retinal barrier that leads to macular edema, and the second is capillary occlusion (ischemia) that leads to a proliferative response. Macular edema is by far the more common of the two and probably the most frequent cause of vision loss in diabetes, Dr. Cunha-Vaz explained.
Edema results in increased retinal volume and occurs in almost every patient, cytotoxic edema that is intracellular, and vasogenic edema that represents breakdown of the blood retinal barrier. Cytotoxic edema, Dr. Cunha-Vaz explained, is a very frequent finding that is underdiagnosed.
Optical coherence tomography (OCT) has proved to be especially helpful to clinicians because it is the only objective measure of retinal thickness and edema. Spectral-domain OCT provides more information about the extent and progression of DME and its effect on central vision, according to Dr. Cunha-Vaz.
"The key worries in DME are the location of the edema in relation to the fovea and its effect on visual acuity and whether the blood-retinal barrier is compromised (Starling's Law)," he said.
Decline in vision begins when the blood-retinal barrier is open.
"The relation between the blood pressure and the tissue pressure is crucial," Dr. Cunha-Vaz continued. "With an increase in blood pressure, the tissue pressure decreases; there is vitreoretinal traction. The tissue osmotic pressure increases in the retinal tissue due to protein accumulation."
Factors he looks for in a clinical examination are the location of the edema in the fovea, the nature of the evolution (acute, chronic, or progressive), status of the blood retinal barrier, signs of retinal pigment epithelial dysfunction, presence of retinal tissue damage, ischemia, vitreoretinal traction, status of metabolic control (HgA1), and blood pressure.
Dr. Cunha-Vaz also emphasized the need to characterize the DME-is the edema focal, diffuse, chronic, or acute? Other factors are the percentage of foveal involvement; the status of the inner and outer blood-retinal barrier; the presence of cysts on OCT, traction, and ischemia; and the HgA1 and blood pressure values.
Treatment includes addressing both systemic factors-such as metabolic control, blood pressure, lipid lowering, and use of possible drugs such as the protein kinase C beta inhibitor ruboxistaurin (Arxxant, Eli Lilly)-and local treatments for an open blood-retinal barrier-such as laser, intra-vitreal antiangiogenetic drugs [pegaptanib (Macugen, OSI/Eyetech); ranibizumab (Lucentis, Genentech)], intravitreal steroids that are administered via drug-delivery implants (Posurdex, Allergan; or Medidur, Alimera Sciences), potential combination treatments, and possibly vitrectomy.