Dear Peter, .PP .fi .na I am fascinated by your question about what causes glaucoma in young patients after vitrectomy. Obviously there are a number of possible explanations: the effect of post-op steroids, something secreted by the vitreous which lowers or something filtered by the vitreous which raises the pressure. There is, however, also a mechanical explanation which I find interesting. I don't wish to stake my reputation on it, but I find it worth while to think about. .PP 1. The blood in the choroidal capillaries and veins is at below intraocular pressure. .br .sp 1.1 The sclera is cannot compress the vortex veins, because .br .sp 1.1.1 The course of the vortex veins is insufficiently tangential to the globe. .br .sp 1.1.2 The sclera is too inelastic to compress the vortex veins. .br .sp 1.2 In patients with light or absent pigment epithelium it is evident on ophthalmoscopy and demonstrable on fluorescein angiography that the choroidal veins are not cylindrical columns, but very thin, flattened strips of blood and are often entirely empty. From the circumstance that at times these vessels can be distended one must infer that their walls are elastic, and that their flattened configuration reflects the circumstance that the extravascular, (intraocular) pressure exceeds the intravascular pressure. .br .sp 1.3 Given that the choroidal and the retinal arteries are supplied by a single vessel, the ophthalmic artery, the much more rapid appearance of fluorescein in the choroidal vessels indicates that the velocity of flow in the choroidal circulation is higher than the velocity of flow in the retinal vessels, with a proportionate transformation of potential into kinetic energy, and a proportionately lower lateral pressure in the choroidal as compared with the retinal vessels. The retinal vein pressure is only marginally higher than intraocular pressure. It is almost certain, therefore, that the choroidal veins are at less than intraocular pressure. .PP 2. The choroidal circulation, being at lower than intraocular pressure acts as a pressure sink which is capable of drawing fluid from the surrounding tissues. .br .sp 2.1 The retina is normally impermeable to water, and in the healthy eye, fluid flows anteriorly through the pupil into the anterior chamber. .br .sp 2.1.1.The pressure gradient between vitreous cavity and choroidal vasculature holds the retina in place, as it were by suction. .br .sp 2.1.2. A retinal hole breaks the suction and permits fluid from the vitreous cavity to be drawn into the choroidal circulation. .br .sp 2.1.3. The loss of suction between retina and choroid as a result of a retinal hole facilitates retinal detachment. .br .sp 2.1.4. The drainage of fluid through the retinal hole into the choroidal circulation in cases of retinal detachment accounts for the lowered intraocular pressure associated with rhegmatogenous (as opposed to traction) retinal detachment. .br .sp 2.1.5. Intraocular inflammation increases the permeability of the retina to water, accounting for the hypotension sometimes associated with uveitis. .br .sp 2.1.6. When the retina become totally permeable to water, the eye is unable to maintain any intraocular pressure, because all intraocular fluids are sucked into the choroidal circulation and phthisis ensues. .br .sp 2.1.6.1. The pathophysiology of phthisis is illuminated by the circumstance that total pupillary occlusion, with no fluid at all passing through the pupil, is compatible with hypotony, strongly suggesting that fluid now leaves the eye through the choroidal vessels. .br .sp 2.1.6.2. The hypothesis that phthitis results from a complete shutdown of aqueous production is not persuasive, since inflammation, abscess or cellulitis almost invariably causes an increase rather than a decrease in the leakage of fluid into the tissues. .br .sp 2.1.6.2.1 The increase of retinal permeability with inflammation and the presence of a large choroidal surface for fluid resorption may be understood, teleologically, as a safety mechanism which prevents the destruction of the eye by the uncompensated increase in tissue pressures which would, in its absence, be caused by inflammation. .br .sp 2.1.6.3. Hydrodynamically it is indifferent whether hypotony is caused by the stoppage of secretion or by reabsorption of the secreted fluids. (Selective) reabsorption of urine is a well-understood principle of renal physiology, and partial reabsorption of aqueous may play a comparably important role in ocular physiology. .PP 3. Choroidal drainage clearly plays a very important role in various pathological situations. The role, if any which choroidal drainage has in controlling the pressure in the healthy eye is unclear. .br .sp 3.1. It has been reported that there is a choroidal outflow through the ciliary body band of the anterior chamber, comprising 30 percent more or less of aqueous secretion. .br .sp 3.1.1. Autoregulation of this choroidal outflow might explain the relative constancy of intraocular pressure in the healthy eye and failure of an autoregulatory mechanism might account for some cases of open angle glaucoma. .br .sp 3.1.2. The pressure (or lack thereof) in the choroidal circulation is in part a function of the cross-sectional shape of the vessels. The cross-sectional shape of the vessels is affected by the intraocular pressure. Theoretically therefore, changes in the cross- section of the choroidal bed caused by intraocular pressure variations might provide a servomechanism for the control of that pressure. .br .sp 3.1.2.1 Upstream compression of the choroidal vasculature will accelerate the velocity of flow and cause a decrease in the pressure of the down-stream choroidal bed. .br .sp 3.1.2.2. Downstream compression of the choroidal vasculature will decrease the velocity of flow in the choroid and will cause and increase in pressure in the upstream choroidal bed. .br .sp 3.1.2.3. Consequently, if a marginal increase in intraocular pressure caused an increase in the velocity of choroidal flow and a decrease in choroidal pressure, negative feedback would obtain, fluid would be drawn into the choroidal vessels and the pressure equilibium of the healthy eye would obtain. .br .sp 3.1.2.4. Similarly, if a marginal increase in intraocular pressure caused a decrease in the velocity of the choroidal flow the choroidal pressure would rise, positive feedback would obtain, and the intraocular pressure would rise. .br .sp 3.1.2.5. Whether a marginal increase in intraocular pressure causes an increase or a decrease in choroidal flow velocity depends on the distribution of the elastic characteristics of the choroidal vessels. .br .sp 3.1.2.6. The pressure lowering effect of vasoactive agents such as epinephrine and timolol might result from their effects in constricting or dilating the choroidal vessels, thereby altering their elastic properties, and altering the effect of marginal increases in intraocular pressure to conform to the equilibrium described in 3.1.2.4. .br .sp 3.1.3. Theoretically a solid vitreous gel, by exerting pressure on the upstream segment of the choroidal vasculature, might serve to increase the velocity of flow and cause a decrease in pressure in the downstream bed. Vitrectomy therefore might be followed by an increase in intraocular pressure. The increase in downstream intravascular pressure after vitrectomy might serve as a stimulus to neovascularization which is sometimes seen in this situation. .br .sp 3.1.4. Theoretically a scleral buckle, to the extent that it deformed and exerted pressure on the downstream choroidal bed, would decrease the velocity of flow and might be expected to be followed by an increase in the intraocular pressure. .br .sp 3.1.5. An increase in intraocular pressure, if it caused a disproportionate compression of the downstream choroidal vasculature, would cause engorgement of the upstream vasculature, with a further increase in pressure. .br .sp 3.1.5.1. Thus there is at least in theory an explanation of open angle glaucoma not as a pathologic alteration of outflow channels but as a disturbance of the mechanism by which the pressure is controlled. .br .sp 3.1.5.2. Since an engorgement of upstream choroidal vessels would be expected to displace the iris anteriorly and to narrow the angle, there is a theoretical explanation for the positive feedback responsible for acute attacks of angle closure glaucoma.