A Newly Defined Vitreous Syndrome Following Cataract Surgery^*: Interpreted According to Recent Concepts of the Structure of the Vitreous, The Seventh Francis I. Proctor Lecture

To compare the incidence of cystoid macular edema (CME) after vitrectomy and CME after phacovitrectomy in patients requiring epiretinal membrane (ERM) removal.

A retrospective, comparative, interventional study.

Medical records of patients who had undergone vitrectomy or phacovitrectomy for ERM removal by a single surgeon were retrospectively reviewed. Phacovitrectomy was performed in all phakic eyes and vitrectomy was performed in all pseudophakic eyes. Increased macular thickness (IMT) was defined as an increase in macular thickness by more than 10% at the postoperative week 4 visit compared to the measurements at baseline.

There were 214 and 53 eyes in the Phacovitrectomy group and the Vitrectomy group, respectively. IMT occurred in 15.4% of the Phacovitrectomy group, which was higher than the incidence of 3.8% in the Vitrectomy group (p=0.023).

IMT, that is suspected to be a type of CME, was not uncommon (15.4%) after phacovitrectomy in phakic eyes but was uncommon (4.8%) after vitrectomy alone in pseudophakic eyes. Irvine-Gass syndrome appears to be triggered by crystalline lens removal itself rather than intraocular surgery or surgical trauma alone.

To investigate the clinical efficacy of dexamethasone vitreous cavity implants (Ozurdex) for the treatment of macular edema (Irvine-Gass Syndrome) after cataract surgery.

Eight patients (eight eyes) with Irvine-Gass syndrome were enrolled for vitreous injections with Ozurdex. The patients included six men (six eyes) and two women (two eyes) with a mean age of 67.12 ± 11.92 years. Changes in the patients best-corrected visual acuity (BCVA), central macular thickness (CMT), and intraocular pressure were compared before and after treatment.

The mean visual acuity BCVA of the patients was 0.81 ± 0.26 before implantation, which improved to 0.20 ± 0.12, 0.13 ± 0.09, and 0.15 ± 0.13 at 2 weeks, 1 month, and 3 months after implantation, respectively (P < 0.001). The patient’s mean CMT before implantation was 703.00 ± 148.88 μm, and it reduced to 258.87 ± 37.40 μm, 236.25 ± 28.74 μm, and 278.00 ± 76.82 μm at 2 weeks, 1 month, and 3 months after implantation, respectively (P < 0.001).

The dexamethasone vitreous cavity implant (Ozurdex) is a safe and effective treatment, which can effectively improve patient’s visual acuity and reduce macular edema associated with cataract surgery.

Besides cystoid macular edema due to a blood-retinal barrier breakdown, another type of macular cystoid spaces referred to as non-vasogenic cystoid maculopathies (NVCM) may be detected on optical coherence tomography but not on fluorescein angiography. Various causes may disrupt retinal cell cohesion or impair retinal pigment epithelium (RPE) and Müller cell functions in the maintenance of retinal dehydration, resulting in cystoid spaces formation. Tractional causes include vitreomacular traction, epiretinal membranes and myopic foveoschisis. Surgical treatment does not always allow cystoid space resorption. In inherited retinal dystrophies, cystoid spaces may be part of the disease as in X-linked retinoschisis or enhanced S-cone syndrome, or occur occasionally as in bestrophinopathies, retinitis pigmentosa and allied diseases, congenital microphthalmia, choroideremia, gyrate atrophy and Bietti crystalline dystrophy. In macular telangiectasia type 2, cystoid spaces and cavitations do not depend on the fluid leakage from telangiectasia. Various causes affecting RPE function may result in NVCM such as chronic central serous chorioretinopathy and paraneoplastic syndromes. Non-exudative age macular degeneration may also be complicated by intraretinal cystoid spaces in the absence of fluorescein leakage. In these diseases, cystoid spaces occur in a context of retinal cell loss. Various causes of optic atrophy, including open-angle glaucoma, result in microcystoid spaces in the inner nuclear layer due to a retrograde transsynaptic degeneration. Lastly, drug toxicity may also induce cystoid maculopathy. Identifying NVCM on multimodal imaging, including fluorescein angiography if needed, allows guiding the diagnosis of the causative disease and choosing adequate treatment when available.