Macular Edema

Book
In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan.
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Excerpt

Macular edema is a retinal condition characterized by fluid buildup in the central part of the retina responsible for sharp, central vision, and accompanies various retinal diseases such as diabetic retinopathy, retinal vascular occlusions, and uveitis. This condition causes decreased visual acuity and, when persistent, can lead to severe vision loss. Fluid accumulates due to a mismatch between retinal fluid entry and exit mechanisms. Dysfunction of the blood-retinal barrier allows the entry of proteins and solutes into retinal tissue, which underlies its pathogenesis.

The distinctive anatomical characteristics of the macula, including its abundant photoreceptor count, elevated metabolic activity, and limited extracellular fluid resorption due to a central avascular zone, along with its specialized cellular and molecular composition containing specific glial cells like Müller cells, suggest a propensity for fluid accumulation. Furthermore, the intriguing arrangement of the Henle fiber layer and the potential presence of a "glymphatic system" further indicate the macula's role as a reservoir for fluid retention.

Patients affected by macular edema commonly experience symptoms such as metamorphopsia, micropsia, blurred vision, central scotoma, and reduced contrast or color sensitivity. Clinicians frequently utilize fundus fluorescein angiography (FFA) and optical coherence tomography (OCT) for diagnostic purposes, as diagnosing macular edema clinically can be challenging in patients with mild disease or when adequate visualization of the fundus is impossible. The visual impairment can be variable and reversed with appropriate therapy. Treatment options for macular edema vary depending on the underlying pathology and may encompass anti–vascular endothelial growth factor therapy (VEGF), corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), or surgical intervention. These treatments target vasoactive and inflammatory mediators that disrupt the blood-retinal barrier.

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