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.
Quantifying HC may help refine ocular pharmacotherapy, as transscleral water movement increases intraocular drug elimination and impedes transscleral drug delivery. The potential scleral outflow is two to three times higher than that which occurs in vivo; hence, medical or surgical interventions that fully exploit this pathway have considerable capacity to lower intraocular pressure.
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