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Ophthalmology – Cystoid Macular Edema (CME)
Cystoid macular edema (CME) is a condition characterized by accumulation of fluid within the retinal layers of the macula, particularly in the perifoveal region, leading to blurred or decreased central vision. It represents a final common pathway of many ocular diseases rather than a single disease entity. The most common form is postoperative CME, especially following cataract surgery.
CME occurs due to breakdown of the blood-retinal barrier, resulting in leakage of fluid into the retinal tissue. Although the exact mechanism is not fully understood, contributing factors include inflammation, vitreous traction, and vascular instability. Fluid accumulates either intracellularly (within Müller cells) or extracellularly, forming characteristic cystic spaces.
Clinically, CME may be asymptomatic or present with blurred vision, decreased visual acuity, or metamorphopsia (distorted vision). It is especially important to ask about recent ocular surgery, as well as systemic conditions such as diabetes, uveitis, or hypertension, and medications like prostaglandin analogs or niacin, which may contribute to its development.
On examination, findings include foveal thickening and cystic changes in the macula. However, mild cases may not be easily visible clinically and require imaging. Optical coherence tomography (OCT) is the most sensitive tool, showing increased retinal thickness and cystic spaces, often in the outer plexiform layer, sometimes with subretinal fluid. Fluorescein angiography (FA) classically demonstrates a “petaloid” pattern of dye leakage in the macula along with optic disc hyperfluorescence.
CME has numerous causes, including:
If CME persists, second-line treatments include periocular or intravitreal corticosteroid injections and intravitreal anti-VEGF agents (e.g., bevacizumab). Additional therapies such as oral acetazolamide may be helpful in select cases. In cases related to structural causes like vitreomacular traction or epiretinal membrane, vitrectomy surgery may be required.
Patients should be monitored every 4–6 weeks with OCT to assess response to treatment. Prognosis is generally good for postoperative CME, especially with early detection and appropriate management. However, chronic or untreated CME can lead to permanent vision loss due to macular damage.
Cystoid macular edema (CME) is a condition characterized by accumulation of fluid within the retinal layers of the macula, particularly in the perifoveal region, leading to blurred or decreased central vision. It represents a final common pathway of many ocular diseases rather than a single disease entity. The most common form is postoperative CME, especially following cataract surgery.
CME occurs due to breakdown of the blood-retinal barrier, resulting in leakage of fluid into the retinal tissue. Although the exact mechanism is not fully understood, contributing factors include inflammation, vitreous traction, and vascular instability. Fluid accumulates either intracellularly (within Müller cells) or extracellularly, forming characteristic cystic spaces.
Clinically, CME may be asymptomatic or present with blurred vision, decreased visual acuity, or metamorphopsia (distorted vision). It is especially important to ask about recent ocular surgery, as well as systemic conditions such as diabetes, uveitis, or hypertension, and medications like prostaglandin analogs or niacin, which may contribute to its development.
On examination, findings include foveal thickening and cystic changes in the macula. However, mild cases may not be easily visible clinically and require imaging. Optical coherence tomography (OCT) is the most sensitive tool, showing increased retinal thickness and cystic spaces, often in the outer plexiform layer, sometimes with subretinal fluid. Fluorescein angiography (FA) classically demonstrates a “petaloid” pattern of dye leakage in the macula along with optic disc hyperfluorescence.
CME has numerous causes, including:
- Post-surgical (most common) – especially after cataract surgery
- Diabetic retinopathy
- Retinal vein occlusion
- Uveitis and retinal vasculitis
- Age-related macular degeneration
- Vitreomacular traction or epiretinal membrane
- Drug-induced (e.g., prostaglandins, tamoxifen)
If CME persists, second-line treatments include periocular or intravitreal corticosteroid injections and intravitreal anti-VEGF agents (e.g., bevacizumab). Additional therapies such as oral acetazolamide may be helpful in select cases. In cases related to structural causes like vitreomacular traction or epiretinal membrane, vitrectomy surgery may be required.
Patients should be monitored every 4–6 weeks with OCT to assess response to treatment. Prognosis is generally good for postoperative CME, especially with early detection and appropriate management. However, chronic or untreated CME can lead to permanent vision loss due to macular damage.
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