The pathophysiology of the anophthalmic socket. Part I. Analysis of orbital blood flow.

A wide variety of complications of the anophthalmic socket develop in patients after enucleation, including enophthalmos, superior sulcus deformities, eyelid malpositions, implant migration and extrusion, poor prosthetic motility, and socket contraction. Changes in the orbital blood flow and metabolic activity of the socket tissues and atrophy of the orbital fat occurring after enucleation have been suggested as two theoretical mechanisms that result in the development of these clinical conditions. Lack of scientific evidence and a limited understanding of the pathophysiologic basis of the features of anophthalmos led us to evaluate the validity of these proposed mechanisms in an animal model. Selected parameters of the normal orbits were compared with the contralateral anophthalmic orbits at different time intervals after surgery. Orbital blood flow was studied with selective ophthalmic artery angiography and radioactive microsphere techniques. Ophthalmic arteriography demonstrated symmetric caliber and filling characteristics of the major orbital vessels of the control and experimental orbits, although their topographic course was slightly more tortuous in the anophthalmic socket. Results of radioactive microsphere analysis of capillary blood flow per weight of the different orbital tissue compartments of the animals in the long-term group showed no significant difference between the normal and anophthalmic sockets. These findings provide evidence that the circulation dynamics and blood flow to orbital tissues do not change after enucleation surgery.