Cystic macular edema

Cystoid macular edema results from fluid accumulation in the outer plexiform and inner nuclear layers of the retina centrally near the foveola, forming fluid-filled cystoid masses. Short-term cystoid macular edema is usually harmless; long-term cystoid macular edema usually results in the coalescence of fluid-containing microcysts into large cystic cavities, followed by formation of a lamellar gap in the fovea and irreversible changes in central vision. Cystoid macular edema is a common and nonspecific condition that may occur with any type of macular edema.

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Causes and Treatment of Cystoid Macular Edema

Pathology of retinal vessels.

• Causes of cystoid macular edema may include diabetic retinopathy, central retinal vein occlusion, idiopathic telangiectasia, central retinal artery macroaneurysm, and radiation retinopathy;
• Laser photocoagulation may be appropriate in some cases.

Intraocular inflammatory process.

• Causes of cystoid macular edema may include peripheral uveitis, Birdshot retinochoroidopathy, multifocal choroiditis with panuveitis, toxoylasmosis, cytomegalovirus retinitis, Behcet's disease, and scleritis;
• Treatment is aimed at controlling the inflammatory process with steroids or immunosuppressive drugs. Systemic administration of carbonic anhydrase inhibitors may be effective in combination with peripheral uveitis.

Post-cataract surgery. Cystoid macular edema is rare after uncomplicated cataract surgery and usually resolves spontaneously.

• Risk factors for cystoid macular edema include anterior chamber intraocular lens implantation, secondary IOL implantation, surgical complications such as posterior capsule rupture, vitreous prolapse and incarceration at the incision site, diabetes, and a history of cystoid macular edema in the fellow eye. The peak incidence of cystoid macular edema is 6-10 weeks postoperatively, although this interval may be much longer;
• Treatment: Elimination of the causes of cystoid macular edema. For example, in case of vitreous impingement in the anterior segment, anterior vitrectomy or vitreous removal with a YAG daser may be performed. The last option for treating this complication is removal of the anterior chamber IOL. If this does not bring results, management of the disease is quite difficult, despite the fact that many cases of cystoid macular edema resolve spontaneously within 6 months. Treatment of persistent cystoid macular edema includes the following measures:
  • Systemic administration of carbonic anhydrase inhibitors.
  • Steroids, either locally or by retrobulbar injection, in combination with nonsteroidal anti-inflammatory drugs such as ketorolac 0.5% (acular) 4 times daily may be effective even in long-standing or clinically significant cystoid macular edema. Unfortunately, in most cases cystoid macular edema recurs when treatment is stopped, so long-term treatment may be necessary. • Pars plana vitrectomy may be performed for cystoid macular edema that is refractory to medical treatment, even in eyes without apparent vitreous pathology.

Condition after surgical procedures

• result of YAG laser capsulotomy, peripheral retinal cryotherapy and laser photocoagulation. The risk of cystoid macular edema is reduced if capsulotomy is performed 6 months or more after cataract surgery. Rarely, cystoid macular edema may develop after scleroplasty, penetrating keratoplasty and glaucoma filtration surgeries;
• Treatment is ineffective, although cystoid macular edema is often mild and resolves spontaneously.

Condition after taking medications

• Causes: local application of 2% adrenaline solution, especially in the aphakic eye, local application of latanoprost and systemic application of nicotinic acid;
• Treatment: discontinue the drug.

Retinal dystrophies

• occurs in retinitis pigmentosa, gyrate atrophy and in the dominantly inherited form of cystoid macular edema;
• Systemic therapy with carbonic anhydrase inhibitors may be effective in cystoid macular edema associated with retinitis pigmentosa.

Vitreomacular traction syndrome is characterized by a partial peripheral detachment of the vitreous body with a strong connection to the macula. This leads to the development of anterior-posterior and tangential traction vectors. In chronic cystoid macular edema due to anterior-posterior traction, vitrectomy can be performed.

Macular epiretinal membrane can sometimes cause cystoid macular edema when perifoveal capillaries are damaged. Surgical removal of the membrane can be effective in some cases.

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Symptoms of Cystoid Macular Edema

The manifestations of cystoid macular edema may vary depending on the cause. Visual acuity may already be reduced as a result of preexisting diseases such as retinal vein occlusion. In other cases (e.g. after cataract removal, in the absence of preexisting diseases), the patient complains of decreased central vision and the appearance of a positive central scotoma.

Fundoscopy reveals no foveal pitting, retinal thickening, and numerous cystic lesions in the neuroepithelium.

In the early stage, cystic changes are difficult to discern and the main finding is a yellow spot in the foveola.

Foveal angiography

• In the arteriovenous phase, moderate parafoveal hyperfluorescence is detected due to early release of the dye.
• In the late venous phase, the intensity of hyperfluorescence increases and individual foci of dye release merge.
• The late venous phase reveals a "flower petal" hyperfluorescence pattern due to accumulation of dye in microcystic cavities of the outer plexiform layer of the retina, which has radially arranged fibers around the center of the foveola (in the layer of Henle).