Histological examination of the eyes, soon after the occlusion of the vortex veins, revealed marked vascular congestion and dilated vessels in the ciliary processes (Figs. 27.1 and 27.2); some eyes even showed the presence of thin-walled blood cysts on the ciliary processes (Figs. 27.3 and 27.4). The area affected depended upon the vortex vein occluded, because each vein had a segmental distribution in the ciliary processes as well. When all the veins were occluded, the fine blood vessels under the ciliary epithelium ruptured in the majority of the eyes within a period of from a few minutes to about 3 h after occlusion. This produced bleeding into the posterior chamber which escaped via the pupil and led to a hyphema in the anterior chamber (Figs. 27.1, 27.2, 27.3, 27.4, 27.5, and 27.6). Histological examination of some of these eyes revealed ciliary epithelial cysts projecting into the posterior chamber (Figs. 27.2, 27.3, and 27.5). When three vortex veins were occluded, such a bleeding was seen in four of nine eyes (or in four of five eyes followed up for more than 24 h), while it was seen in two of twelve eyes on occluding two vortex veins, but in none after occlusion of one vortex vein. In eyes with occlusion of two or three vortex veins, the hyphema was not only less common but also less marked than after occlusion of four veins. The hyphema cleared in the former eyes in a week and in the latter in 2–5 weeks. The occurrence of hyphema with occlusion of all the vortex veins was also seen in studies with vortex vein occlusion in rabbits by others [2, 3, 9], but not observed in dogs [12].

In all the eyes of this series, immediately after occlusion, and before the appearance of any hyphema, thick protein-rich fluid extended from the ciliary processes in the sector drained by the occluded vortex vein (Figs. 27.2, 27.3, and 27.4); this exudate coated the anterior surface of the lens. In the anterior chamber, the protein-rich aqueous resulted in the formation of a gelatinous cobweb-like deposit in its dependent part (Fig. 27.7). It would thus appear that a marked rise in blood pressure in the capillaries of the ciliary processes results in the outpouring of protein-rich aqueous. This was due to the breakdown of the blood-aqueous barrier. Soon after the injection of intravenous fluorescein, profuse leakage of fluorescein, from the involved sector only, was seen; this was at first localized to the involved sector of the pupil and anterior chamber but progressively became more prominent and diffuse (Fig. 27.7). The blood, protein-rich aqueous, and fluorescein from the posterior chamber passed through the pupil on to the anterior lens surface and anterior chamber, but none was seen in the vitreous or on the posterior lens surface. The vitreous in all eyes was clear. On follow-up, the protein-rich aqueous cleared with the return to normal of the uveal circulation.

The iris-lens diaphragm moved forward significantly in eyes with occlusion of all or three vortex veins, because there was an increase in the volume of the posterior compartment of the eye, due to marked venous congestion in the choroidal vascular bed. This resulted in a shallow anterior chamber – shallower after occlusion of all the vortex veins than after three veins (Fig. 27.8). On follow-up, in three of six eyes with all the vortex veins occluded, the anterior chamber was found to be absent after the hyphema had cleared and it never reformed, while in the remaining three eyes, the depth of the anterior chamber became nearly normal after the hyphema had cleared. In eyes with occlusion of one or two vortex veins, no significant change in the depth of the anterior chamber was noticed. The findings of Koster [9] were similar.

As mentioned above, vortex vein occlusion was originally designed to produce raised intraocular pressure and glaucoma [1–11]. In my series [16], eyes with occlusion of all or three vortex veins showed a marked rise in the intraocular pressure immediately after occlusion – about 40–60 mmHg after occlusion of all the vortex veins and about 30–40 mmHg after occlusion of three vortex veins – but no significant rise in intraocular pressure was recorded after occlusion of two or one. This rise in pressure was not related to hyphema, because the intraocular pressure rose as much in eyes without as those with hyphema. Similarly, the protein-rich aqueous seemed to play no role in the rise in intraocular pressure, because the eyes with occlusion of one or two vortex veins had a large amount of gelatinous deposit in the anterior chamber without any rise in the intraocular pressure. In the eyes with elevated intraocular pressure, the angle of the anterior chamber was very narrow, and it could have been blocked in most of them by a forward shift in the iris-lens diaphragm and engorgement of the ciliary body and iris, because of marked venous congestion in the entire uveal tissue.

On the day after the occlusion, the intraocular pressure was either the same as or even higher than the immediate post-occlusion pressure. After 1 week a fall in the intraocular pressure had set in, so that it returned to near normal in eyes with occlusion of all the vortex veins and to unrecordable low levels in eyes with occlusion of three vortex veins; in the eyes with occlusion of all the veins, intraocular pressure then dropped to an unrecordable level in 2 weeks. Having reached the lowest level, the intraocular pressure started to recover; this occurred within 2 weeks after occlusion of three vortex veins. In eyes with occlusion of all the vortex veins, however, the recovery of the intraocular pressure depended upon the state of the anterior chamber, i.e., if the anterior chamber was absent, the eye had permanent marked hypotony, but if the anterior chamber was present, the recovery started after an interval of more than 2 weeks. The intraocular pressure in these eyes did not recover completely but remained subnormal during the period of follow-up. Histological studies showed evidence of atrophy of the ciliary processes and ciliary body in these eyes (Figs. 27.9 and 27.10).

The iris was markedly hyperemic soon after the occlusion of all or three vortex veins (Fig. 27.6). With occlusion of one to three vortex veins, there was sectoral hyperemia of the iris corresponding to the occluded vortex veins. Other authors reported similar findings [2, 9, 12].

On follow-up, three eyes with all the veins occluded and an absent anterior chamber had anterior and posterior synechiae with iris atrophy and iris neovascularization (Fig. 27.11), the clinical appearance resembling that of an eye with long-standing chronic anterior uveitis or anterior segment ischemia. In one of the eyes with three vortex veins occluded, posterior synechiae and sectoral iris atrophy were present. Koster [9] also found these changes in eyes after occlusion of all the vortex veins in rabbits.

In all the eyes, the lens, soon after occlusion of the various vortex veins, had a proteinous deposit on its anterior surface (Fig. 27.7). During a follow-up period of up to 4 weeks, the deposit cleared without leaving any lens abnormalities in any eye except those with all the vortex veins occluded. During follow-up, all the eyes with all the vortex veins occluded showed pigment deposit on the anterior lens surface; in three of these eyes with an absent anterior chamber and permanent ocular hypotony, the lens became completely cataractous within 5 weeks (Fig. 27.12). The changes appeared at first in the anterior cortex of the lens and later resulted in a complete cataract 14, 19, 38, and 90 days after the occlusion. The cataractous change is evidently secondary to impaired nutrition due to degeneration of the ciliary epithelium and ciliary body, as shown by histological studies.

Epithelial edema was seen when the intraocular pressure was very high, in eyes with all or three vortex veins occluded. On follow-up, stromal clouding and vascularization by radial vessels from the limbus were seen in three eyes with all the vortex veins occluded. Two of these had no anterior chamber. Koster [9] also noticed a similar corneal vascularization after occlusion of all the vortex veins and likened it to that of interstitial keratitis, with a gradually progressive pannus from the limbus toward the center. I feel that the corneal changes are secondary to the changes in the intraocular pressure and anterior chamber.

The degenerative changes seen in the lens and anterior segment of the eye in these monkeys (particularly in those with occlusion of all the vortex veins) very much resemble those seen in patients with long-standing anterior uveitis or anterior segment ischemia. Almost all the pathologic changes in the anterior segment of the monkey eyes depend upon the changes in the anterior chamber (e.g., protein-rich aqueous, hyphema, shallow or absent anterior chamber), which in turn are secondary to marked disturbances of the uveal circulation associated with the changes in the ciliary processes and the forward displacement of the iris-lens diaphragm, by engorgement of the posterior uveal vascular bed increasing the volume of the posterior segment.