Vitrectomy for diabetic macular traction and edema associated with posterior hyaloidal traction.

Diabetic macular edema: pathogenesis and treatment.

Diabetic maculopathy is characterized by the accumulation of extracellular fluid in Henle's layer and the inner nuclear layer of the retina. The localization of the edema is likely to be due, in part, to the relative barrier properties of the inner and outer plexiform layers. The origin of the extracellular fluid is from the intravascular compartment. Although changes to retinal blood flow may partly explain the extravasation of fluid, the most important mechanism is breakdown of the blood retinal barriers. Both the inner blood retinal barrier formed by the retinal capillary endothelial cell tight junctions and the outer barrier formed by the retinal pigment epithelial cell tight junctions can be affected. The mechanism of breakdown of the blood retinal barriers is likely to be changes to the tight junction proteins including occludin and ZO-1. The biochemical messenger inducing these changes may be vascular endothelial growth factor. The origin of this or other cofactors may be the retinal glial cells. The underlying biochemical stimulus to the production of vascular endothelial growth factor is chronic hyperglycaemia, but it is uncertain by what pathway this is effected.

The Pathogenesis of Edema in Diabetic Maculopathy

Morphometric analysis of CNS microvascular endothelium

• Multiple short argon laser pulses can coagulate the retinal pigment epithelium selectively, while sparing the adjacent neural retina and choroid; in contrast, continuous-wave laser irradiation typically damages the neural retina and choroid. The healing response to selective photocoagulation of the retinal pigment epithelium was studied in rabbits during a period of 4 weeks. The lesions were never visible ophthalmoscopically. During the healing period, the epithelium was reformed by a single sheet of hypertrophic retinal pigment epithelial cells. In contrast to continuous-wave photocoagulation, only minimal inflammatory response was found. Retinal pigment epithelial cells showed clear signs of viability, eg, phagocytized outer segments. The local edema in the photoreceptor layer and subretinal space found in the early stage disappeared when the blood-retinal barrier was reestablished. The choriocapillaris remained unaffected. No subsequent damage to the photoreceptors was found. This type of photocoagulation may be useful for retinal pigment epithelium—related diseases, eg, diffuse diabetic macular edema.

Response of the Retinal Pigment Epithelium to Selective Photocoagulation

• Rats with experimental diabetes (induced by streptozocin [Streptozotocin]) were studied by vitreous fluorophotometry and horseradish peroxidase tracer technique Vitreous fluorescein sodium concentration notably increased four to eight days after a single dose of streptozocin No leakage from the retinal vasculature could be demonstrated by the horseradish peroxidase tracer study, but three types of retinal pigment epithelial (RPE) lesions were observed The RPE lesions seemed to be partially responsible for the increase of vitreous fluorescein concentration

Chi-Yen Shih

Papers

Clinicopathologic Study of Blood-Retinal Barrier in Experimental Diabetes Mellitus