Current evidence of pathophysiology of diabetic macular edema: A review

Abstract

Diabetic macular edema (DME) is an important cause of vision loss in patients with diabetes mellitus. The pathophysiology of DME can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the events that cause the edema to become chronic. On a macrocellular level, DME is believed to be in part caused by alterations in hydrostatic and oncotic pressures and shear stress. Angiogenic factor expression, inflammation and oxidative stress constitute the key components of microvascular pathways. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. Macular edema is thought to be caused as a result of these consequences.

Keywords: Diabetes mellitus, Macular edema, Pathophysiology, Vascular endothelial growth factor, Inflammation

Core tip: Diabetic macular edema (DME) is an important cause of vision loss in patients with diabetes mellitus. The pathophysiology of DME can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the events that cause the edema to become chronic. On a macrocellular level, DME is believed to be in part caused by alterations in hydrostatic and oncotic pressures and shear stress. Angiogenic factor expression, inflammation and oxidative stress constitute the key components of microvascular pathways. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. Macular edema is thought to be caused as a result of these consequences.