Macular Edema, Pseudophakic (Irvine-Gass) Treatment & Management

  • Author: David G Telander, MD, PhD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Apr 21, 2010
 

Medical Care

Treatment is aimed at the underlying etiology; however, several of the common treatments may help different causes of cystoid macular edema (CME).

Medical treatment modalities include the following:

  • Corticosteroids directly inhibit the enzyme phospholipase, blocking the formation of prostaglandins. They are considered the primary treatment of CME in many instances, specifically in the treatment of CME secondary to uveitis. Corticosteroids can be administered topically or orally; they can also be injected intravitreally (off-label use) or injected into the sub-Tenon space (off-label use). However, corticosteroids have many systemic and ocular adverse effects, and some patients become intolerant to them as a result.
  • NSAIDs inhibit the enzyme cyclooxygenase and can be used in the prevention and treatment of CME.
    • NSAIDs are usually administered topically for approximately 3-4 months and on an as-needed basis.
    • In a large, multicenter, prospective, double-masked, study of ketorolac versus placebo in the treatment of 120 patients with chronic aphakic or pseudophakic CME, statistically significant improvement in visual acuity occurred in patients that received ketorolac versus placebo.[1]
  • The RPE is important in the maintenance of the blood-retinal barrier and in the prevention of a surplus of extracellular and intracellular fluid within the retina. The enzyme carbonic anhydrase is present on the apical and basal surfaces of the RPE cell membrane. Carbonic anhydrase inhibitors (CAIs), such as acetazolamide, enhance the pumping action of RPE cells, facilitating the transport of fluid across the RPE.
  • Bevacizumab has been used for the treatment pseudophakic CME. Vascular endothelial growth factor (VEGF) is a known mediator of capillary leakage implicated in the pathogenesis of diabetic retinopathy and exudative age-related macular degeneration. Bevacizumab (Avastin) is a monoclonal antibody able to inactivate the effects of VEGF. The role VEGF has in pseudophakic CME is not clear, yet several authors have reported resolution of CME after administration of bevacizumab for their patients retrospectively. However, one report by Spitzer et al did not see any beneficial effects with this treatment.[2] Prospective studies are needed.
  • When vitreous is captured in the corneal wound following complicated cataract surgery, YAG laser lysis of the vitreous strands has been used with some success.
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Surgical Care

Surgical therapy includes pars plana vitrectomy (PPV).

  • PPV is useful in the treatment of cystoid macular edema (CME) in several instances, as follows:
    • Remove vitreous strands tracking to the surgical wound or pupil status after complicated ocular surgery or trauma.
    • Peeling of the posterior hyaloid face from the surface of the macula in vitreomacular traction syndrome or chronic CME cases unresponsive to medical treatment.
    • Peeling of epiretinal membranes from the surface of the macula when associated with CME.
    • Removal of inflammatory mediators from the vitreous cavity.
    • Removal of retained nuclear lens fragments.
    • Repositioning of a dislocated or subluxed IOL.
  • Multiple studies have reported improvement of CME after PPV in cases of aphakic, pseudophakic, or uveitis-related CME. Some surgeons advocate the peeling of the internal limiting membrane during the PPV.
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Diet

While diets high in antioxidants have been shown to be beneficial to the retina in age-related macular degeneration, no dietary change has been shown to influence the resolution of postoperative pseudophakic macular edema. Active diabetic retinopathy and the dietary implications of uncontrolled hyperglycemia have been associated with higher rates of diabetic macular edema, which can be worsened by the inflammation of cataract surgery causing more significant pseudophakic CME.

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Contributor Information and Disclosures
Author

David G Telander, MD, PhD  Assistant Professor, Department of Ophthalmology and Vision Science, Division of Vitreo-Retinal Diseases and Surgery, University of California Davis School of Medicine

David G Telander, MD, PhD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, American Society of Cataract and Refractive Surgery, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher T Cessna, DO  Vitreo-Retinal Specialist, Geisinger Health System

Christopher T Cessna, DO is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Brian A Phillpotts, MD  Former Vitreo-Retinal Service Director, Former Program Director, Clinical Assistant Professor, Department of Ophthalmology, Howard University College of Medicine

Brian A Phillpotts, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, and National Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Steve Charles, MD  Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians & Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society

Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

References

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Fundus photo of the right eye in a patient with cystoid macular edema.
Fluorescein angiography of the right eye (late phase) showing central macular leakage in cystic spaces around the fovea.
Optical coherence tomography (OCT) of the right eye showing central macular cystic spaces in cross-section.
Fundus photo of the right eye in a patient with cystoid macular edema from diabetic retinopathy.
Fluorescein angiography of the right eye (late phase) showing central macular leakage in cystic spaces around the fovea.
Optical coherence tomography (OCT) of the right eye showing central macular cystic spaces in cross-section.
 
 
 
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