Pseudophakic (Irvine-Gass) Macular Edema Treatment & Management

Updated: Sep 25, 2018
  • Author: David G Telander, MD, PhD; Chief Editor: Michael Taravella, MD  more...
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Medical Care

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


Corticosteroids directly inhibit the enzyme phospholipase, blocking the formation of prostaglandins and leukotrienes. 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). [15, 16] However, corticosteroids have many ocular adverse effects, including cataract formation or elevated IOP. Therefore, some patients cannot tolerate them.

Patients with diabetes may benefit from a dexamethasone intravitreal implant (0.7 mg). [17] This treatment has also shown benefit in patients without diabetes. [18, 19]

Nonsteroidal anti-inflammatory drugs (NSAIDs)

NSAIDs inhibit the enzyme cyclooxygenase and can be used in the prevention and treatment of CME. [20] They are usually administered topically for approximately 3-4 months and on an as-needed basis. Topical NSAIDs have not been found to cause elevated IOP or cause cataract formation.

In a large, multicenter, prospective, double-masked, study of ketorolac versus placebo in the treatment of 120 patients with chronic aphakic or pseudophakic CME, a statistically significant improvement in visual acuity occurred in patients who received ketorolac versus placebo. [21]

Newer NSAIDs, such as bromfenac, may increase compliance and efficacy, as it requires only once-a-day dosing.

Nepafenac is unique because it is a prodrug and is activated only after diffusing into the vitreous of the eye. This drug has been shown in animal models to have higher ocular penetration. [22] The clinical benefit of this increased penetration has yet to be shown, as comparative large clinical trials have yet to be done.

A Cochrane review of 7 studies examined the effectiveness of NSAIDs in the treatment of CME following cataract surgery. Two of the studies demonstrated a positive effect of ketorolac on chronic CME. However, none of the remaining 5 trials revealed a significant difference between comparative groups. [23]

Carbonic anhydrase inhibitors (CAIs)

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. CAIs, such as acetazolamide, enhance the pumping action of RPE cells, facilitating the transport of fluid across the RPE. [24]

Antivascular endothelial factor (anti-VEGF)

If the macular edema is associated with diabetic retinopathy, the therapy is targeted at the causative molecule vascular endothelial growth factor (VEGF). VEGF is a known mediator of capillary leakage implicated in the pathogenesis of diabetic retinopathy and exudative age-related macular degeneration.

Anti-VEGF therapy (ie, ranibizumab) has been shown in many clinical trials to be superior to laser alone for diabetic macular edema. [25]

Anti-VEGF therapy (bevacizumab) has been used for the treatment pseudophakic CME. Bevacizumab 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. [26] Prospective studies are needed. More recently, combination therapy (intraocular steroids with anti-VEGF agents) can be effective in treating refractory pseudophakic CME. [27]


Surgical Care

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.

If vitreous adhesion to the surgical wound is evident, YAG laser to sever these connections can be helpful. Alternately, pars plana vitrectomy (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, chronic, or uveitis-related CME. [28, 29] Some surgeons advocate the peeling of the internal limiting membrane during the PPV. Proceed to Medication.



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.



The risk of cystoid macular edema (CME) can be decreased by avoiding intraoperative complications, such as posterior capsule rupture, vitreous loss, vitreous to the wound, iris prolapse, or dislocated lens.

Perioperative and preoperative NSAIDs may decrease the incidence of CME associated with cataract surgery. [30]

Many studies have shown that preoperative and perioperative drops and medications can decrease the incidence of postoperative pseudophakic cystoid macular edema. Specifically, topical steroids and NSAIDs can be effective at decreasing the occurrence of CME. [31] Additional studies have shown that intraocular steroid injections (anti-VEGF) are very effective in high-risk patients, such as those with diabetic retinopathy.


Further Outpatient Care

Patients with cystoid macular edema (CME) are treated on an outpatient basis with regular follow-up visits to monitor for any signs of clinical improvement.

If steroids are used as a treatment, it is critical to closely monitor intraocular pressure, as glaucoma is a serious complication.