Irvine–Gass syndrome

Overview

Irvine–Gass syndrome, also known as pseudophakic cystoid macular edema (CME), is a condition characterized by the accumulation of fluid in the macula, the central part of the retina responsible for sharp vision, following cataract surgery. First described by Irvine in 1953 and later detailed with fluorescein angiography by Gass in 1969, this syndrome is one of the most common causes of visual impairment after otherwise successful cataract extraction. It typically presents within weeks to months after surgery and can cause blurry or decreased central vision.

Causes

Irvine–Gass syndrome occurs due to inflammation and breakdown of the blood-retinal barrier after cataract surgery, leading to fluid leakage and cyst formation in the macula. Contributing factors include:

• Post-surgical inflammation: Even with modern surgical techniques, minor inflammation can trigger the condition.

• Capsular rupture or complications during surgery

• Pre-existing ocular conditions: Such as uveitis, diabetic retinopathy, or retinal vein occlusion.

• Use of intraocular lenses (IOLs): Especially in the earlier generations of implants.

• Prostaglandin analog eye drops: May increase the risk when used soon after surgery.

Symptoms

The symptoms of Irvine–Gass syndrome usually develop gradually and may include:

• Blurred or decreased central vision

• Distortion of vision (metamorphopsia): Straight lines may appear wavy or bent.

• Reduced contrast sensitivity

• Difficulty with tasks requiring sharp vision: Such as reading or recognizing faces.

• Usually painless: Unlike infectious or severe inflammatory complications.

In some cases, especially mild ones, it may be detected on imaging before symptoms are noticeable.

Diagnosis

Diagnosis of Irvine–Gass syndrome involves a thorough eye examination and imaging tests to confirm the presence of macular edema:

• Fundoscopy: May show subtle signs of retinal thickening or cystic spaces in the macula.

• Optical coherence tomography (OCT): The gold standard for diagnosing and monitoring CME. It visualizes fluid-filled cysts within the retinal layers.

• Fluorescein angiography: Shows characteristic petaloid or flower-petal leakage patterns in the macula due to capillary permeability.

• Visual acuity testing: To assess functional impact and monitor changes over time.

Treatment

Treatment for Irvine–Gass syndrome focuses on reducing inflammation and resolving macular edema to restore vision. Options include:

• Topical anti-inflammatory medications:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs): e.g., ketorolac or nepafenac.

  • Corticosteroids: e.g., prednisolone acetate drops.

• Oral or periocular steroids: Used in more severe or persistent cases.

• Intravitreal injections: Of corticosteroids or anti-VEGF agents may be required in refractory or chronic cases.

• Avoidance of prostaglandin analogs: In glaucoma patients post-surgery, alternative medications are considered.

Most cases respond well to conservative treatment, but some may require long-term therapy or combination approaches.

Prognosis

The prognosis for Irvine–Gass syndrome is generally favorable, especially when treated early. Most patients experience significant improvement in vision with appropriate therapy. In mild cases, the condition may resolve spontaneously over several weeks to months. However, in persistent or untreated cases, chronic macular edema can lead to permanent visual impairment. Regular follow-up with OCT imaging is essential to monitor treatment response and prevent long-term complications.