Purpose: To determine whether uveal effusion syndrome (UES) is caused by altered scleral permeability to water and large molecules.
Methods: Transscleral water movement was measured using surgically removed sclera clamped in a modified Ussing chamber and connected to a water column set at intraocular pressure. Sclera was also clamped between two hemichambers, and transscleral diffusion of FITC-dextrans (4.4-77 kDa) was measured with a spectrophotometer. Clinical data were prospectively collected using postal questionnaires.
Results: Ten patients (mean age, 63 years; mean spherical equivalent, +4.7 D) had a median preoperative visual acuity of 0.20 that improved to 0.33 after surgery. Nine eyes showed visual improvement, three worsened, and two were unchanged. Histology showed disorganization of collagen fibrils, with amorphous deposits expanding the interfibrillary spaces. The mean thickness (+/-1 SD) of the excised scleral specimens was 585 +/- 309 microm, and the mean specific hydraulic conductivity was 23.9 +/- 27.5 x 10(-14) cm(2), compared with 5.8 +/- 3.9 x 10(-14) cm(2) in age-matched control specimens (P = 0.068). Three specimens had hydraulic conductivity above the 95% CI of the controls. Control eyes showed a significant reduction in diffusion coefficient (D) with age. Eyes had a mean D of 5.69 +/- 5.35 x 10(-8) cm(2) x s(-1), similar to control eyes (6.14 +/- 2.40 x 10(-8) cm(2) x s(-1), 20 kDa dextran). In one eye, the result was higher than the 95% CI of the control; in three, it was lower.
Conclusions: UES is not caused by reduced scleral hydraulic conductivity, which tends to be higher than expected. Reduced macromolecular diffusion may impede the normal transscleral egress of albumin with subsequent osmotic fluid retention in some, but not all eyes.