Age

There is a modest decline in outflow facility with age.248–250 This decline appears to counterbalance a similar decrease in aqueous humor formation. Histologic studies indicate a number of agerelated changes in the trabecular meshwork, including thickening and fusion of the trabecular sheets, degeneration of collagen and elas­ tic fibrils, accumulation of wide-spacing collagen, loss of endothelial cells, hyperpigmentation of the endothelial cells, accumulation of

intracellular organelles, accumulation and alteration of extracellular matrix, and decrease in the number of giant vacuoles.251–254

Hormones

A number of investigators have postulated that endogenous glu­ cocorticoids regulate aqueous humor outflow.255 Corticosteroids administered topically, systemically, or periocularly are capable of reducing outflow facility. The response to corticosteroids appears to be genetic in part and is greater in certain groups, including patients with primary open-angle glaucoma (POAG) and their first-degree relatives, myopic patients, and diabetic patients. This subject is reviewed at length in Chapter 18. Other hormones, such as progesterone,256,257 thyroxin,258 relaxin, and chorionic gona­ dotropin,258 have been postulated to influence outflow facility in physiologic or pharmacologic doses. Other active substances, such

as prostaglandins, substance P, and angiotensin, may affect aqueous outflow.259,260

Ciliary muscle tone

Increased tone of the ciliary muscle increases total outflow facil­ ity. The increased tone can be the result of accommodation,261,262

electrical stimulation of the oculomotor nerve, posterior depres­ sion of the lens,28,29,181 or administration of parasympathomimetic

drugs such as pilocarpine.206 The increased muscle tone pulls the scleral spur posteriorly and internally, which opens the intertrabec­ ular spaces and Schlemm’s canal (see Fig. 3-3).

Drugs

Pilocarpine and other cholinergic agents increase outflow facility.206 Adrenaline (epinephrine) and dipivefrin and other adrenergic

agonists increase both conventional and unconventional out­ flow.230,231,263,264 The parasympatholytic agents and the ganglionic

blocking agents reduce outflow facility. Prostaglandins increase uveoscleral outflow.207–211 Alpha agonists decrease aqueous produc­

tion and increase uveoscleral outflow.265 Bradykinin was noted to increase outflow facility in one study.266

Surgical therapy

Argon laser trabeculoplasty improves outflow facility. Cataract extrac­ tion and penetrating keratoplasty reduce outflow facility temporar­ ily, perhaps by deforming the trabecular meshwork and reducing its

support.267 Cyclodialysis, as mentioned previously, increases uveo­ scleral outflow.129,195

Diurnal fluctuation

There has been considerable controversy about whether or not there is a diurnal fluctuation of outflow facility.255,268,269

Glaucoma

Outflow facility is reduced in most forms of glaucoma. This can occur through a variety of mechanisms, depending on the type of glaucoma. In primary infantile glaucoma, the outflow structures develop improperly (see Ch. 19). In angle-closure glaucoma, the peripheral iris is pushed or pulled against the trabecular meshwork, preventing aqueous humor from reaching the outflow channels (see Chs 15 and 16).The trabecular meshwork can also be covered by a membrane, as in epithelial downgrowth, neovascular glaucoma, or the iridocorneal endothelial syndrome.

In the secondary open-angle glaucomas, the trabecular meshwork can be obstructed by a variety of particulate matter, including red blood cells, white blood cells, tumor cells, ghost cells, zonular frag­ ments (after -chymotrypsin), pigment particles, and lens particles (see Ch. 18).The meshwork can also be obstructed by non-particulate foreign matter, such as lens protein and viscoelastic substances.

There is great controversy about the fundamental defect of the outflow channels in POAG. A variety of theories have been proposed to explain the decreased outflow facility of this disease, including (1) an accumulation of foreign material in the trabecular meshwork; (2) a loss of trabecular endothelial cells; (3) a collapse of Schlemm’s canal, and (4) an obstruction of the collector channels. This subject is discussed at length in Chapter 17.

Episcleral venous pressure

Aqueous humor leaving the eye by trabeculocanalicular outflow eventually passes into the venous system.The pressure in the veins that receive the aqueous humor is referred to as episcleral venous pressure.

Episcleral venous pressure can be measured by a variety of techniques, including pressure chambers,234,270–275 torsion balance devices,271,276 force displacement transducers, air jets,270 and direct

cannulation.178 Most studies of normal human eyes find episcleral venous pressure to be in the range of 8–11.5 mmHg (Table 3-3). The venous pressure levels are affected by body position but do not vary in constant fashion from quadrant to quadrant of the eye.

Most studies find no correlation between episcleral venous pressure and age,249,275 although there is one conflicting report.274

Table 3-3  Episcleral venous pressure in human eyes

There is considerable controversy about whether episcle­ ral venous pressure is altered in glaucoma (excluding those cases of secondary glaucoma caused by elevated episcleral venous pres­

sure). Some investigators report similar episcleral venous pressure levels in normal and glaucomatous eyes,277,280 whereas others

report lower episcleral venous pressure in glaucomatous and ocular hypertensive eyes (see Table 3-3).276,279,281 It should be emphasized

that even in the studies that find lower episcleral venous pressure in glaucomatous eyes, the differences in pressure are small: the largest reported mean difference between glaucomatous patients and nor­ mal individuals is approximately 2 mmHg.279 From this it is clear that episcleral venous pressure is not a factor in the pathogenesis of POAG. Elevated episcleral venous pressure can be the cause of secondary glaucoma in a number of conditions that are reviewed in Chapter 18.

There are a number of experimental techniques described for raising episcleral venous pressure. The most commonly used

method in humans is to place a cuff about the neck with sufficient pressure to impede venous return.249,282 Under these conditions,

IOP rises by about 0.8 mmHg for every 1 mmHg increase in epis­ cleral venous pressure.When episcleral venous pressure is raised by some disease process, IOP is usually increased as well. However, the relationship between the pressure increases is more complex in the chronic situation than in the acute experimental situation. Many conditions (e.g., carotid cavernous fistula) that increase episcleral venous pressure also cause ocular ischemia, which reduces aque­ ous humor formation and IOP.283 Furthermore, acute elevations of episcleral venous pressure increase the facility of outflow, whereas chronic elevations may produce secondary changes in the angle structures and decrease the outflow facility (see Ch. 18).282

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