Macular edema

Tranos, Paris; Wickremasinghe, Sanjeewa; Stangos, Nikos T.; Topouzis, Fotis; Tsinopoulos, Ioannis; Pavésio, Carlos

doi:10.1016/j.survophthal.2004.06.002

Cited by 132 publications

(127 citation statements)

References 162 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…Macular edema represents the common final pathway of many intraocular and systemic diseases as a nonspecific sign usually involving the retinal vessels [1,2]. While the progression of symptoms is usually slow, patients may still experience a sudden onset, depending on the etiology.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of Macular Edema

Scholl¹,

2010

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%

Pathophysiology of Macular Edema

Scholl¹,

2010

View full text Add to dashboard Cite

show abstract

“…Structural alterations of the macula occur after intraocular surgery or may develop in the presence of ocular or systemic diseases [1,2,6]. The pathophysiology is attributed to the induced inflammation, which destabilizes the blood-retina barrier [3].…”

Section: Discussionmentioning

confidence: 99%

“…The final common pathway of inflammation after ocular procedures appears to be the increased perifoveal capillary permeability and breakdown of the blood-retina barrier, resulting in accumulation of fluid in the outer plexiform and inner nuclear layers of the retina [3]. This condition is referred to as cystoid macular edema (CME) or Irvine-Gass syndrome [4,5,6]. …”

Section: Introductionmentioning

confidence: 99%

Prospective Study of Foveal Thickness Alterations after Cataract Surgery Assessed by Optical Coherence Tomography

Tsilimbaris

Diakonis²,

Kymionis³

et al. 2012

Ophthalmologica

View full text Add to dashboard Cite

Background/Aims: To evaluate the alterations of mean foveal thickness (MFT) and visual acuity (VA) outcomes after uncomplicated cataract surgery in different groups of patients. Methods: This study included eyes of consecutive patients who underwent cataract surgery between November 2007 and June 2009. The patients included in the study were divided into 4 groups, as follows: history-free patients, patients with diabetes mellitus without macular involvement at baseline, patients with glaucoma, and patients with epiretinal membrane (ERM). Preoperatively and at 1, 3 and 6 months postoperatively, patients were evaluated for MFT by optical coherence tomography at the central 1-mm macular zone and for logarithm of the minimum angle of resolution best spectacle-corrected VA (BSCVA). Results: A total of 202 eyes were included in the study. MFT values demonstrated a statistically significant increase (p < 0.01) after cataract surgery in all groups at the first and third postoperative month. The history-free (p = 0.09) and glaucoma (p = 0.19) groups did not demonstrate a statistically significant difference in MFT values between the preoperative and 6-month measurements. MFT values 6 months after cataract surgery in the diabetes and ERM groups remained significantly higher (p < 0.01). Despite these findings, VA increased significantly (p < 0.01) in all groups at all postoperative follow-ups. Conclusions: MFT values increased significantly in all groups at the first and third months after cataract surgery. At 6 months, MFT values returned to preoperative levels in the history-free and glaucoma patients, while they remained significantly higher in the diabetic and ERM patients. Despite these macular alterations, BSCVA improved significantly after cataract surgery in all groups at all postoperative follow-ups.

show abstract

“…Cystoid macular edema (CME) is a well-known complication of anterior segment surgery and was first described by Irvine in 1953 [112,113]. Angiographic CME may occur in 20% of patients who undergo uncomplicated phacoemulsification or extracapsular extraction [112,[114][115][116] , but only 1% of these patients experience a significant visual acuity decrease [112,117,118].…”

Section: Cystoid Macular Edemamentioning

confidence: 99%