Uveitis and Macular Edema: A Complex Relationship
Uveitis and Macular Edema: A Complex Relationship
Uveitic macular edema is obviously a complex condition. The treatment modalities listed above have in common an anti-inflammatory component. One must wonder whether a history of uveitis (which appears clinically to be in remission) is, in actuality, a marker for subclinical inflammation, control of which results in improvement of the macular edema.
Making the matter even more complex is that patients with uveitis commonly develop abnormalities at the vitreoretinal interface, with traction, epiretinal membrane formation or other, more subtle interactions, as described by Bouchenaki and colleagues. These investigators analyzed the vitreoretinal interface by OCT in patients with Fuchs heterochromic iridocyclitis and found vitreoretinal modifications in 90% of affected eyes. The main vitreoretinal interactions were vitreous hyperreflective dots (45%), thickening of posterior hyaloid (38.7%), posterior vitreous detachment (32.3%), vitreoretinal traction (29%), and epiretinal membrane (25.8%).
Salcedo and associatesconducted similar studies on 90 eyes of 53 patients with pars planitis, finding epiretinal membrane in 28 eyes (31.1%), vitreomacular tractional syndrome in 10 eyes (11.1%), cystoid macular edema in 5 eyes (5.5%), retinal detachment in 1 eye (1.1%), and retinal fibrosis in 3 eyes (3.3%). Of the 28 eyes that had epiretinal membrane, 11 had persistent angiographic macular edema unresponsive to treatment. Of the 62 eyes that did not present epiretinal membrane, 10 developed persistent macular edema. The investigators concluded that there is an association between epiretinal membrane and persistent macular edema.
Cereda and associates came to the same conclusion. They evaluated the efficacy of pars plana vitrectomy with peeling of epiretinal membrane and internal limiting membrane (PPVP) in the management of chronic uveitic macular edema sustained by macular pucker in 34 eyes of 34 patients with cystoid macular edema and macular pucker secondary to chronic intermediate or posterior uveitis that was unresponsive to medical treatment. The primary outcome was change in visual acuity at 1, 2, 3, 4, 5, and more than 5 years after surgery. Secondary outcomes measures were change in mean thickness of the central fovea area (1 mm of diameter) as measured on OCT at preoperative examination and at last follow-up; changes in inflammation were recorded as cell count in anterior chamber (ACc) and vitreous (Vc) at 1, 2, 3, 4, 5, and more than 5 years after surgery. All 34 patients had at least 1 year of follow-up; 27 patients had 2 years of follow-up, 22 had 3 years, 13 had 4 years, 10 had 5 years, and 4 had more than 5 years of follow-up. Compared with baseline (0.7 logMAR SD ± 0.4) a significant gain in mean visual acuity was found at 1 year (0.4 logMAR SD ± 0.3) (paired T test: P <.0001), 2 years (pre-op: 0.75 logMAR SD ± 0.4 and post-op: 0.35 logMAR SD ± 0.3) (P < .0001), and 3 years (pre-op 0.75 logMAR SD ± 0.45 and post-op 0.45 logMAR SD ± 0.4). Mean foveal thickness was 392 μm (SD ± 125μm) at preoperative examination, decreasing to a mean of 276 μm (SD ± 54μm) at last follow-up (paired T test: P < .001). ACc remained stable, whereas Vc was statistically significantly lower compared to ACc during the first 5 years of follow-up (Wilcoxon: P < .05 at 1, 2, 3, 4, 5 years).
Cereda and associates concluded that PPVP in patients with macular edema and macular pucker secondary to chronic uveitis has a significant beneficial effect on visual function for at least 3 years and on foveal thickness and vitreous haze up to 5 years after surgery.
Macular edema in patients with uveitis is an incredibly complex and frustrating matter, with at least 4 possible causes of the edema:
Thoughtful specialists will have to consider all of these possibilities and address each if they are to have any hope of solving the problem and improving patients' vision.
The Inflammation Connection
Uveitic macular edema is obviously a complex condition. The treatment modalities listed above have in common an anti-inflammatory component. One must wonder whether a history of uveitis (which appears clinically to be in remission) is, in actuality, a marker for subclinical inflammation, control of which results in improvement of the macular edema.
Making the matter even more complex is that patients with uveitis commonly develop abnormalities at the vitreoretinal interface, with traction, epiretinal membrane formation or other, more subtle interactions, as described by Bouchenaki and colleagues. These investigators analyzed the vitreoretinal interface by OCT in patients with Fuchs heterochromic iridocyclitis and found vitreoretinal modifications in 90% of affected eyes. The main vitreoretinal interactions were vitreous hyperreflective dots (45%), thickening of posterior hyaloid (38.7%), posterior vitreous detachment (32.3%), vitreoretinal traction (29%), and epiretinal membrane (25.8%).
Salcedo and associatesconducted similar studies on 90 eyes of 53 patients with pars planitis, finding epiretinal membrane in 28 eyes (31.1%), vitreomacular tractional syndrome in 10 eyes (11.1%), cystoid macular edema in 5 eyes (5.5%), retinal detachment in 1 eye (1.1%), and retinal fibrosis in 3 eyes (3.3%). Of the 28 eyes that had epiretinal membrane, 11 had persistent angiographic macular edema unresponsive to treatment. Of the 62 eyes that did not present epiretinal membrane, 10 developed persistent macular edema. The investigators concluded that there is an association between epiretinal membrane and persistent macular edema.
Cereda and associates came to the same conclusion. They evaluated the efficacy of pars plana vitrectomy with peeling of epiretinal membrane and internal limiting membrane (PPVP) in the management of chronic uveitic macular edema sustained by macular pucker in 34 eyes of 34 patients with cystoid macular edema and macular pucker secondary to chronic intermediate or posterior uveitis that was unresponsive to medical treatment. The primary outcome was change in visual acuity at 1, 2, 3, 4, 5, and more than 5 years after surgery. Secondary outcomes measures were change in mean thickness of the central fovea area (1 mm of diameter) as measured on OCT at preoperative examination and at last follow-up; changes in inflammation were recorded as cell count in anterior chamber (ACc) and vitreous (Vc) at 1, 2, 3, 4, 5, and more than 5 years after surgery. All 34 patients had at least 1 year of follow-up; 27 patients had 2 years of follow-up, 22 had 3 years, 13 had 4 years, 10 had 5 years, and 4 had more than 5 years of follow-up. Compared with baseline (0.7 logMAR SD ± 0.4) a significant gain in mean visual acuity was found at 1 year (0.4 logMAR SD ± 0.3) (paired T test: P <.0001), 2 years (pre-op: 0.75 logMAR SD ± 0.4 and post-op: 0.35 logMAR SD ± 0.3) (P < .0001), and 3 years (pre-op 0.75 logMAR SD ± 0.45 and post-op 0.45 logMAR SD ± 0.4). Mean foveal thickness was 392 μm (SD ± 125μm) at preoperative examination, decreasing to a mean of 276 μm (SD ± 54μm) at last follow-up (paired T test: P < .001). ACc remained stable, whereas Vc was statistically significantly lower compared to ACc during the first 5 years of follow-up (Wilcoxon: P < .05 at 1, 2, 3, 4, 5 years).
Cereda and associates concluded that PPVP in patients with macular edema and macular pucker secondary to chronic uveitis has a significant beneficial effect on visual function for at least 3 years and on foveal thickness and vitreous haze up to 5 years after surgery.
Macular edema in patients with uveitis is an incredibly complex and frustrating matter, with at least 4 possible causes of the edema:
Persistent subclinical inflammation;
Vitreomacular mechanical interactions;
Frank membrane formation on the macular surface; or
Retinal pigment epithelial ion pump dysfunction as a consequence of damage from previous chronic inflammation.
Thoughtful specialists will have to consider all of these possibilities and address each if they are to have any hope of solving the problem and improving patients' vision.
