DME management requires attention to details

Managing diabetic macular edema (DME) means focusing on a number of details to obtain a good clinical picture of each patient's status, emphasized José Cunha-Vaz, MD, PhD. Dr. Cunha-Vaz described how he approaches this patient population in his 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," said Dr. Cunha-Vaz.

Four metabolic alterations are relevant to macular edema: hyperglycemia; endothelial damage, permeability, and proteinuria; angiogenesis; and changes in the blood components. All of these factors are permanent in patients with diabetes, he noted.

The basic elements in DME are edema that 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 frequently underdiagnosed.

Optical coherence tomography has proved to be especially helpful to clinicians because it is the only objective measure of retinal thickness and edema.

"The key worries in DME are the location of the edema, its effect on visual acuity, and whether the blood retinal barrier is compromised [Starling's Law]," he said.

If the blood retinal barrier is open, the decline in the vision starts.

"The relation between blood pressure and tissue pressure is crucial," Dr. Cunha-Vaz explained. "With an increase in blood pressure, the tissue pressure decreases and there is vitreoretinal traction. With a decrease in plasma osmotic pressure, the tissue osmotic pressure increases and there is protein accumulation in the retinal tissue."

The factors he ascertains in patients are: the location of the edema in the fovea; the nature of the evolution (acute, chronic, progressive); the status of the blood retinal barrier; the signs of retinal pigment epithelial dysfunction; the presence of retinal tissue damage; ischemia; vitreoretinal traction; the status of metabolic control (HgA1C); and blood pressure.

Treatment includes addressing both systemic factors-such as metabolic control, blood pressure, lipid lowering, and medications, such as protein kinase C and ruboxistaurin (Eli Lilly)-and local treatment, such as laser; intravitreal antiangiogenetic drugs (pegaptanib [Macugen, Pfizer Ophthalmics]; ranibizumab [Lucentis, Genentech]); intravitreal steroids, such as with one proprietary implant (Medidur, Alimera Sciences); potential combination treatments; and possibly vitrectomy.