Macular edema is defined as an accumulation of fluid in the outer plexiform layer and the inner nuclear layer as well as a swelling of Müller cells of the retina. It consists of a localized expansion of the retinal extracellular space (sometimes associated with the intracellular space) in the macular area. Macular edema is a common cause of a sudden or chronic decrease in visual acuity occurring in many ocular diseases such as age-related macular degeneration, diabetic retinopathy and retinal vein occlusion. As a nonspecific sign of many intraocular and systemic diseases, macular edema represents a common final pathway. The existence of the blood-retinal barrier (BRB) formed by intercellular junctions is the precondition required to maintain this physiological status. This status may become severely disturbed by many diseases, finally resulting in macular edema. In this article, the development of macular edema will also be classified by its pathophysiological and pathobiochemical pathways. Vascular components, the dysfunctional BRB, the role of proteins and water fluxes as well as the role of several inflammatory mediators (e.g. angiotensin II, vascular endothelial growth factor, prostaglandins) in the retina will be discussed as responsible mechanisms leading to the development of macular edema.
Macular edema represents a common final pathway for many ocular diseases. Related ocular disorders include diabetic retinopathy, vascular occlusions, postsurgical situations, and uveitic diseases. The key pathophysiologic process is a breakdown of the blood-retinal barrier, normally preventing water movement in the retina, thus allowing fluid to accumulate in the retinal tissue via special water fluxes. Inflammatory processes and an increase in vascular permeability play a central role. Different mechanisms, complicated by ischemic conditions, interact in a complex network. Key factors are angiotensin II, prostaglandins, and the vascular endothelial growth factor. The various pathogenetic mechanisms and their contribution to the edema process are described in detail in this article.
Choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD) is now the leading cause of blindness and severe vision loss among people over the age of 40 in the Western world. Its prevalence is certain to increase substantially as the population ages. Treatments currently available for the disease include laser photocoagulation, verteporfin photodynamic therapy, and intravitreal injections of corticosteroids and anti-angiogenic agents. Many studies have reported the benefits of each of these treatments, although none is without its risks. No intervention actually cures AMD, nor the neovascularization associated with it. However, its symptoms are treated with varying degrees of success. Some treatments stabilize or arrest the progress of the disease. Others have been shown to reverse some of the damage that has already been done. These treatments can even lead to visual improvement. This paper will review the major classes of drugs and therapies designed to treat this condition.
In recent years, new drugs against retinal diseases have been developed consisting mainly of steroid or anti-vascular endothelial growth factor compounds. Targeting macular edema, the second shows a possible therapeutic role in the proliferative form of diabetic retinopathy, requiring further investigation. New biodegradable delivery systems show an advantage in sustaining effective compound concentrations for longer times and have positive impact on safety profile and cost-effectiveness of the drug, a factor of grave importance when considering the future of any new drug in the market. All these new therapeutic approaches alone or in combination with the existing treatments have to demonstrate their efficacy and safety in diabetic retinopathy in current and future trials.
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