Postvitrectomy hypotonia: the role of the vitreous and retinochoroidal lesions.

The pathomechanisms of hypotonia after vitrectomy remain obscure. To examine the possible escape of intraocular fluid through the ocular wall, hydraulic fluid conductivity was measured across preparations of retina, pigmented epithelium, and choroid isolated from rabbit eyes 1, 3, 5, or 7 weeks after the production of laser or cryopexy lesions. The hydraulic conductivity measured in a modified Fischbarg-Bourguet chamber, was 0 in controls. At 1 and 3 weeks after transpupillary diode laser coagulation of the equatorial retina, hydraulic conductivity was measurable. However, the conductivity of these preparations returned to 0 by 5 weeks. After transscleral cryopexy, conductivity remained elevated for 7 weeks. Break-up of residual cortical vitreous with hyaluronidase increased the conductivity of "mature" cryopexy lesions to the values obtained 1 week after injury. These results suggest that there is escape of fluid across retinochoroidal lesions; fluid conductance typically decreases over time; an intact cortical gel can hinder conductance and seal the retinochoroidal leak. Thus, the risk factors for hypotonia appear to include extensive retinochoroidal lesions and the absence of a normal cortical vitreous in aphakia and/or after aggressive vitrectomy.