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Symptoms ⬇

Decreased vision.

Signs ⬆ ⬇

(See Figures 11.14.1 to 11.14.3.)

Critical

Irregularity and blunting of the foveal light reflex, macular thickening with or without small intraretinal cysts in the foveal region.

Other

Vitreous cells, optic nerve swelling, and dot hemorrhages may be observed depending upon etiology of CME.

11-14.3 Optical coherence tomography of cystoid macular edema.

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11-14.2 Intravenous fluorescein angiography of cystoid macular edema.

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11-14.1 Cystoid macular edema.

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Etiology ⬆ ⬇

Work Up ⬆ ⬇

Workup
  1. History: Recent intraocular surgery? Diabetes? Previous uveitis or ocular inflammation? Night blindness or family history of eye disease? Medications, including topical epinephrine, dipivefrin, or prostaglandin analogs?
  2. Complete ocular examination, including gonioscopy to rule out the presence of retained lens fragments following cataract surgery and haptic malposition of implanted anterior chamber intraocular lens. Thorough peripheral fundus evaluation (scleral depression inferiorly may be required to detect pars planitis). Macular examination is best performed with a slit lamp and a 60- or 90-diopter lens, fundus contact lens, or a Hruby lens.
  3. IVFA shows early leakage of perifoveal capillaries and late macular staining, classically in a petaloid or spoke-wheel pattern. Optic nerve head leakage is sometimes observed (Irvine–Gass syndrome). Fluorescein leakage does not occur in select cases of pseudo-CME (see above).
  4. OCT can be utilized to document the presence of CME and demonstrate the efficacy of therapy. OCT outlines the loss of foveal contour resulting from enlarged cystic spaces within the retina and thickening of the macula.
  5. Other diagnostic tests when indicated: Fasting blood sugar and hemoglobin A1c, ERG, others.
NOTE:

Subclinical CME commonly develops after cataract extraction and is noted on IVFA (angiographic CME). OCT shows no CME and these cases are not treated.

Treatment ⬆ ⬇

Treat the underlying disorder if possible. For CME related to specific etiologies (e.g., diabetes, retinal vein occlusion, intermediate uveitis, etc.), see specific sections.

  1. Topical NSAID (e.g., ketorolac 0.5% q.i.d., bromfenac 0.09%, or nepafenac 0.3% daily) often in conjunction with topical steroids (e.g., prednisolone acetate 1% q.i.d.).
  2. Discontinue topical epinephrine, dipivefrin, or prostaglandin analog drops and medications containing nicotinic acid.
  3. Other forms of therapy are often used to treat CME depending upon etiology:
    • Subtenon steroid (e.g., triamcinolone 40 mg/mL, inject 0.5 to 1.0 mL).
    • Intravitreal steroid (e.g., triamcinolone 40 mg/mL, inject 1 to 4 mg).
    • Intravitreal anti-VEGF therapy (e.g., bevacizumab 1.25 mg in 0.05 mL).
    • Systemic steroids (e.g., prednisone 40 mg p.o. daily for 5 days and then taper over 2 weeks).
    • Systemic NSAIDs (e.g., indomethacin 25 mg p.o. t.i.d. for 6 weeks).
    • Topical or systemic carbonic anhydrase inhibitors (e.g., dorzolamide 2% t.i.d. or acetazolamide 500 mg p.o. daily starting dose) in cases of RP-associated CME.
    • CME with or without vitreous incarceration in a surgical wound may be improved by vitrectomy or YAG laser lysis of the vitreous strand.

Follow Up ⬆

Postsurgical CME patients should be started on a topical NSAID and a topical steroid with follow up in 4 to 6 weeks to determine response to topical drop therapy. Other forms of CME should be followed in a similar time frame to monitor response to initial therapy.