Ординатура / Офтальмология / Английские материалы / Clinical Pathways in Glaucoma_Zimmerman, Kooner_2001
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100Primary Angle-Closure Glaucoma
•Peripheral site, especially if Nd:YAG used, to avoid damage to the underlying crystalline lens.
•Use the 2 or 10 o’clock position, so that the iridectomy is under the upper lid, but not the 12 o’clock position, where gas bubbles formed during the procedure can obscure visualization and interfere with completion of the laser procedure. Also, avoid creation of an iridectomy in the interpalpebral fissure (3 or 9 o’clock position) where postlaser visual symptoms and inadvertent laser damage to the macula are more likely.50
•If the procedure is going well and a second iridectomy can be made easily, some surgeons elect to perform a second iridectomy in case the first one becomes occluded later. This delayed closure is an unusual occurrence following Nd:YAG iridectomy for primary angle closure. Delayed closure is a more common problem following argon laser iridectomy, but can even occur after Nd:YAG iridectomy, especially for certain secondary angle closures such as neovascular glaucoma, uveitic glaucoma, or aphakic/ pseudophakic pupillary block.
What General Guidelines Are Useful
in Nd:YAG Laser Iridectomy?
The Nd:YAG laser is useful for initial laser iridectomy and particularly for completion of unsuccessful attempts at argon laser iridectomy. One should choose a site of thin iris as far in the periphery as clear visibility permits. In the periphery of the iris, damage to the underlying crystalline lens is least likely. Precise focusing is crucial to successful Nd:YAG iridectomy, so areas of arcus senilis should be avoided, as well as visible iris blood vessels to minimize hyphema during and after the procedure. Usually, one to five single shots of 4 to 7 mJ
Table 5–7. Argon Laser Iridectomy Techniques
“Gas bubble” technique for light blue irises (Hoskins and Migliazzo46)
1.Create a 1.5-mm gas bubble on the surface of the iris with 1500 mW, 50 m, 0.2–0.5 second burn (hold down the foot pedal until the desired bubble forms)
2.Immediately apply one or two additional shots, as needed, focused on the apex of the bubble; the gas bubble’s inner surface will re-reflect laser energy toward the iris; this will usually achieve penetration, as evidenced by a plume of brown iris pigment carried by aqueous from the posterior chamber into the anterior chamber
3.Lower laser settings to 500–1000 mW, 50 m, 0.05 seconds, and use multiple shots to enlarge and “clean up” the iridectomy
Modified “chipping away” technique for dark brown irises
In these eyes the areas of laser application tend to fill in with surrounding iris tissue after each shot, much like trying to dig a hole in dry sand; use many highpower, short-exposure burns: 1500 mW, 50 m, 0.02–0.05 seconds
“Drumhead” technique for intermediate iris colors (Simmons and Deppermann47)
1.Tighten the proposed iridectomy site like a drumhead by surrounding it with four “stretch” burns: 100–200 mW, 200 m, 0.2 seconds
2.Penetrate iris with 500 mW, 50 m, 0.5 second burns
3.“Clean up” site with 500 mW, 50 m, 0.05 second burns
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each are required. Some surgeons prefer to use the Nd:YAG burst mode for iridectomy. However, because with most instruments the procedure can be completed with single shots, many avoid the use of the burst mode, just in case it might increase the chance of damaging the underlying crystalline lens.
Active bleeding from the iris is common during Nd:YAG iridectomy, and may interfere with completion of the laser procedure. It can be temporarily controlled with the intermittent application of firm pressure upon the eye with the hand-held laser contact lens. Some surgeons minimize iris bleeding by pretreating the iridectomy site with argon laser photocoagulation.51,52 A typical method used for such pretreatment is to tighten the desired site in similar fashion to the “drumhead” iridectomy technique, by surrounding it with four spaced burns of approximately 200 mW, 200 m, and 0.2 seconds and then coagulating the central area with 10 to 20 burns of 400 to 800 mW, 100 m, and 0.1 seconds.47 The applications should be sufficient to tighten the iridectomy site without causing excessive pigment disruption. However, bleeding from the Nd:YAG iridectomy site very rarely causes significant problems.
It is not necessary to enlarge a small Nd:YAG iridectomy after penetration. Nd:YAG iridectomies tend to be smaller but “cleaner” than those made with the argon laser and are less prone to subsequent closure. Also, damage to the underlying lens capsule is more likely if additional photodisruption is used once a patent iridectomy has been achieved.
What Should Be Done After Laser Iridectomy?
The very important evaluation and management of the eye following iridectomy, as diagrammed in Figure 5–5, is seldom discussed and is often neglected. After laser iridectomy has relieved pupillary block, it is crucial to reexamine the eye and repeat the gonioscopy. The IOP may be improved following iridectomy, but there is much work yet to do. One-fourth of these eyes will require further treatment for glaucoma at some time in the future. In addition, 40 to 80% of fellow eyes of eyes with acute angle-closure glaucoma will have an acute attack within 5 to 10 years if they are not treated with prophylactic iridectomy. The pain and emotional upset resulting from an acute angle-closure attack in the first eye may increase sympathetic flow, induce pupillary mydriasis, and increase relative pupillary block, precipitating an acute attack of angle closure in the fellow eye during treatment of the first eye. Prophylaxis with 0.5 to 1% pilocarpine in the fellow eye is used by some, but it is not foolproof and, in some cases, can increase relative pupillary block and angle closure/closability. Prompt laser iridectomy in the fellow eye, if its angle is closed/closable, is necessary.53,54 If the angle closure is truly unilateral, one should consider the differential diagnosis of secondary angle closure in the first eye, as listed in Table 5–1.
What If, Following Iridectomy, the IOP
Is Down and the Angle Is Open and Not Closable?
Proceed with laser iridectomy to relieve relative pupillary block in the fellow eye if its angle is closable as shown in Figure 5–5.
102 Primary Angle-Closure Glaucoma
Caution: Just because the IOP is improved following iridectomy and the angle is open, do not assume that the iridectomy is patent, especially if the argon laser has been used. The pupillary block may have been relieved by peaking of the pupil due to shrinkage of iris tissue from argon laser applications, even if penetration of the iris is incomplete. This pupilloplasty effect is usually transient, so be certain of a patent iridectomy to avoid recurrence of relative pupillary block and angle closure. Conversely, a permanent spontaneous “cure” of pupillary block-induced angle closure can occur due to a sector of stromal iris atrophy resulting from the ischemia of an acute attack that alters the lens/iris interface, thereby permanently relieving relative pupillary block.
What If, After Iridectomy, the IOP
Remains Elevated with Fresh Peripheral Anterior Synechiae Following Medical Therapy
and Laser Iridectomy for Acute Angle Closure?
Fresh peripheral anterior synechiae can occasionally be broken with laser peripheral iris gonioplasty and/or operative goniosynechialysis. Gonioplasty creates surface iris burns to shrink and flatten the iris tissue and pull it away from the trabecular meshwork.23 Operative goniosynechialysis has been reported to break fresh synechiae and improve facility of outflow up to 1 year following an acute attack of primary angle closure.21,22
What If, After Iridectomy, the Angle Remains Closed/
Closable from Plateau Iris Syndrome?
With plateau iris syndrome the angle is still appositionally closed/closable after iridectomy, which eliminates relative pupillary block but not the plateau iris mechanism. Remember that most cases of angle closure with plateau iris configuration, as seen gonioscopically prior to iridectomy, are actually due to increased relative pupillary block, which is cured by iridectomy. To resolve plateau iris syndrome, where angle closability persists after iridectomy, one must flatten the peripheral iris to remove it from the proximity of the trabecular meshwork with chronic miotic therapy or laser peripheral iris gonioplasty.
CHRONIC MIOTIC THERAPY FOR PLATEAU IRIS SYNDROME
Chronic miotics were the only available therapy for the prevention of progressive synechia formation in plateau iris syndrome prior to the introduction of argon laser gonioplasty. Chronic miotic therapy, such as pilocarpine 0.5 to 1% every 12 hours, is much less convenient, less well tolerated, and less dependable than laser gonioplasty, however. Dapiprazole (Rev Eyes), which achieves miosis by -adrenergic blockade, may offer an alternative, but at this time it is costly and has a relatively short shelf life following its reconstitution.
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LASER PERIPHERAL IRIS GONIOPLASTY
FOR PLATEAU IRIS SYNDROME
Laser peripheral iris gonioplasty, as outlined in Table 5–6, is the preferred method of relieving the plateau iris mechanism.55,56 With this technique, argon laser burns are applied to the peripheral iris roll to shrink and pull it away from the angle. The effect is often transient, and retreatment is often necessary. Therefore, it is imperative that these eyes are followed indefinitely with periodic gonioscopy.
Remember that plateau iris syndrome may develop years after iridectomy, so periodic gonioscopy should be performed on all patients who have had iridectomy for primary angle closure.
What If, After Iridectomy, the IOP Remains Elevated
Without Fresh Peripheral Anterior Synechiae and
In the Absence of Plateau Iris Syndrome?
In this situation, one should proceed to medical therapy, laser trabeculoplasty, and filtration surgery, as needed for control of IOP of this open angle component of the patient’s “mixed mechanism” glaucoma.
Treat IOP with medical glaucoma therapy just as with chronic open angle glaucoma. If medical therapy is unsuccessful, consider laser trabeculoplasty, depending on the desired and existing IOP, the extent of optic nerve and visual field damage, and the fraction of the circumference of trabecular meshwork available for trabeculoplasty. For example, if the pressure is 26, the desired pressure is 18, and 11 clock hours of trabecular meshwork are available for trabeculoplasty, then it is a reasonable option. On the other hand, if the pressure is 45, the desired pressure is 16, and only 2 clock hours of meshwork are visible, then laser is a waste of time and may pose a hazard. In actual practice, most cases lie in between these two extremes and the surgeon must exercise his or her judgment as to the value of laser trabeculoplasty in the particular setting. As a general rule, potentially dangerous posttrabeculoplasty IOP elevation should be minimized by treating no more than half of the visible trabecular meshwork at a single laser session.
If medications and laser trabeculoplasty fail to control the IOP, filtration surgery is necessary.
What Particular Problems Does Filtration Surgery Pose
in These Eyes?
Glaucoma filtration operations in eyes with primary angle closure can be exceedingly challenging and fraught with unique problems. In the characteristically small, hyperopic and deep-set eyes with primary angle closure, surgical exposure is usually far less than optimal. If the eye has recently had an acute attack of angle closure, visibility of anterior segment anatomy is often decreased by the presence of corneal edema. Also, conjunctival hyperemia predisposes to intraoperative bleeding, further compromising visibility. This is
104 Primary Angle-Closure Glaucoma
complicated by a small anterior segment in which to maneuver. In addition to these technical problems, there is an increased risk of intraoperative suprachoroidal hemorrhage and of postoperative malignant (ciliary block) glaucoma.
Future Considerations
The treatment of glaucoma in general, and therefore that of primary angleclosure glaucoma, will evolve and improve. As more glaucoma drugs have emerged, expanding the medical therapeutic options, the fraction of patients unable to use medications because of expense, inconvenience, and side effects has decreased. In particular, the continued development of aqueous suppressant medications increase the options for the ophthalmologist to lower the intraocular pressure even in the face of synechial angle closure. As the understanding of neuroprotectve medications grows, patients with primary angle closure, just like those with other forms of glaucoma, will benefit from medications that enhance the optic nerve’s ability to resist pressure-induced damage.
Through the years, instrumentation and techniques for laser iridectomy have continued to improve. Although Nd:YAG laser iridectomy is, at present, a wonderful procedure for patient and physician, iridectomy technology will doubtless become even better.
Relative pupillary block and the beneficial effect of laser iridectomy are very well understood. In contrast, plateau iris syndrome, despite recent progress, remains an enigma. A better understanding of the mechanics of plateau iris will yield a wider and more efficacious array of therapeutic options than laser gonioplasty and chronic miotics.
Finally, and perhaps most important, a better understanding and wider appreciation of the demographics of primary angle closure will increase awareness of the problem and lead to earlier detection, before permanent synechial angle closure and optic nerve damage occur.
References
1.Duke-Elder S, Jay B: Glaucoma. In: System of Ophthalmology, Vol II. St. Louis: CV Mosby, 1969:380.
2.Barkan O: Glaucoma: classification, causes, and surgical control. Results of microgonioscopic research. Am J Ophthalmol 1938;21:1099–1113.
3.Becker S: Clinical gonioscopy—a text and stereoscopic atlas. St. Louis: CV Mosby, 1972:1–3, 81–107.
4.Mapstone R: Mechanics of pupil block. Br J Ophthalmol 1968;52:19–25.
5.Patel KH, Javitt JC, Tielsch JM, et al: Incidence of acute angle-closure glaucoma after pharmacologic mydriasis. Am J Ophthalmol 1995; 120(6):709–717.
6.Ritch R: Plateau iris is caused by abnormally positioned ciliary processes. Glaucoma 1992; 1:23–26.
7.Tornquist R: Angle-closure glaucoma in an eye with a plateau type of iris. Acta Ophthalmol 1958;36:419-423.
8.Wand M, Grant WM, Simmons RJ, Hutchinson BT: Plateau iris syndrome. Trans Am Acad Ophthalmol Otolaryngol 1977; 83:122–130.
9.Pavlin CJ, Ritch R, Foster FS: Ultrasound biomicroscopy in plateau iris syndrome. Am J Ophthalmol 1992;113:390–395.
10.Congdon N, Wang F, Tielsch JM: Issues in the epidemiology and population-based screening of primary angle closure glaucoma. Surv Ophthalmol 1992;36(6):411–423.
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11.Drance SM: Angle closure glaucoma among Canadian Eskimos. Can J Ophthalmol Symposium 1973;8:252–254.
12.Cox JE: Angle closure glaucoma among the Alaskan Eskimos. Glaucoma 1984;6:135–137.
13.Arkell SM, Lightman DA, Sommer A, et al: The prevalence of glaucoma among Eskimos of NW Alaska. Arch Ophthalmol 1987;105:482–485.
14.Clemmensen V, Alsbirk PH: Le glaucome primarie du Groenland. Bull Soc Ophtalmol Fr 1969;82:243–249.
15.Clemmensen V, Alsbirk PH: Primary angle closure glaucoma in Greenland. Acta Ophthalmol (Copenh). 1971;49:47–58.
16.Alsbirk PH: Primary angle closure glaucoma: oculometry, epidemiology and genetics in a high risk population. Acta Ophthalmol 1976;54(127):5–31.
17.Quigley HA: Number of people with glaucoma worldwide. Br J Ophthalmol 1996;80:389–393.
18.Campbell DG: A comparison of diagnostic techniques in angle closure glaucoma. Am J Ophthalmol 1979; 88:197–204.
19.Forbes M: Gonioscopy with corneal indentation. A method for distinguishing between appositional closure and synechial closure. Arch Ophthalmol 1966;76:488–492.
20.Forbes M: Indentation gonioscopy and efficacy of iridectomy in angle closure glaucoma. Trans Am Ophthalmol Soc 1974; 72:488–515.
21.Campbell DG, Vela A: Modern goniosynechialysis for the treatment of synechial angle closure glaucoma. Ophthalmology 1984;91:1052–1060.
22.Shingleton BJ, Chang MA, Bellows AR, Thomas JV: Surgical goniosynechialysis for angle-clo- sure glaucoma. Ophthalmology 1990;97(5):551–556.
23.Wand M: Argon laser gonioplasty for synechial angle closure. Arch Ophthalmol 1992;110: 363–367.
24.Mapstone R: Provocative tests in closed angle glaucoma. Br J Ophthalmol 1976;60:115–119.
25.Wand M: Provocative tests in angle-closure glaucoma: a brief review with commentary. Ophthalmic Surg 1974;5:32–37.
26.Patel KH, Javitt JC, Tielsch JM, et al: Incidence of acute angle closure glaucoma after pharmacologic mydriasis. Am J Ophthalmol 1995;120:709–717.
27.Chandler PA, Trotter RR: Angle-closure glaucoma. Subacute types. Arch Ophthalmol 1955;53: 305–317.
28.van Herick W, Shaffer RN, Schwartz A: Estimation of width of angle of anterior chamber. Incidence and significance of the narrow angle. Am J Ophthalmol 1969;68:626–629.
29.Bonomi L, Marchini G, DeFranco I, et al: Effects of topical dapiprazole on the intraocular pressure in humans: a controlled study. Glaucoma 1988;10(1):8–10.
30.Reibaldi A: A new alpha blocking agent. Glaucoma 1984;3(6):255–257.
31.Wand M, Grant WM: Thymoxamine hydrochloride: an alpha-adrenergic blocker. Surv Ophthalmol 1980;25:75–84.
32.Halasa AH, Rutkowski PC: Thymoxamine therapy for angle closure glaucoma. Arch Ophthalmol 1973;90:177–179.
33.Anderson DR: Corneal indentation to relieve acute angle-closure glaucoma. Am J Ophthalmol 1979; 88:1091–1093.
34.Kimbrough RL, Stewart RH, Okereke PC: The management of refractory acute angle closure glaucoma. Glaucoma 1987;9:125–127.
35.Ritch R: Argon laser treatment for medically unresponsive attacks of angle-closure glaucoma. Am J Ophthalmol 1982; 94:197–204.
36.Simmons RJ, Savage JA, Belcher CD, Thomas JV: Usual and unusual uses of the laser in glaucoma. In: Symposium on the Laser in Ophthalmology and Glaucoma Update: Transactions of the New Orleans Academy of Ophthalmology. St. Louis: CV Mosby, 1985:154–175.
37.Chandler PA, Simmons RJ: Anterior chamber deepening for gonioscopy at time of surgery. Arch Ophthalmol 1965;74:177–190.
38.Shaffer RN: Operating room gonioscopy in angle closure glaucoma surgery. Trans Am Ophthalmol Soc 1957;55:59–66.
39.Quigley HA: Long term follow-up of laser iridotomy. Ophthalmology 1981;88:218–224.
40.Robin AL, Pollack IP: A comparison of neodymium:YAG and argon laser iridotomies. Ophthalmology 1984;91:1011–1016.
41.Brainard JO, Landers JH, Shock JP: Recurrent angle closure glaucoma following a patent 75micron laser iridotomy: a case report. Ophthalmic Surg 1982;13:1030–1032.
42.Robin AL: The role of apraclonidine in laser therapy for glaucoma. Trans Am Ophthalmol Soc 1989;87:729–761.
43.Kolker AE: Techniques of argon laser iridectomy. Trans Am Ophthalmol Soc 1984;82:302–306.
44.Pollack IP: Use of argon laser energy to produce iridotomies. Ophthalmic Surg 1980;11: 506–525.
45.Robin A, Pollack IP: Argon laser peripheral iridotomies in the treatment of primary angle closure glaucoma. Long-term follow-up. Arch Ophthalmol 1982;100:919–923.
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46.Hoskins HD, Migliazzo CV: Laser iridectomy—a technique for blue irises. Ophthalmic Surg 1984;15:488–490.
47.Belcher CD: Laser iridectomy. In: Belcher CD, Thomas JV, Simmons RJ (eds): Photocoagulation in Glaucoma and Anterior Segment Surgery. Baltimore: Williams & Wilkins, 1984:99
48.Klapper RM: Q-switched neodymium:YAG laser iridotomy. Ophthalmology 1984;91:1017–1021.
49.Latina MA, Puliafito CA, Steinert RR, Epstein DL: Experimental iridotomy with the Q-switched neodymium:YAG laser. Arch Ophthalmol 1984;102:1211–1213.
50.Berger BB: Foveal photocoagulation from laser iridotomy. Ophthalmology 1984;91:1029–1033.
51.Fleck BW, Wright E, McGlynn C: Argon laser pretreatment 4 to 6 weeks before Nd:YAG iridotomy. Ophthalmic Surg 1991;22(11):644–649.
52.Goins K, Schmeisser E, Smith T: Argon laser pretreatment in Nd:YAG iridotomy. Ophthalmic Surg 1990;21(7):497–500.
53.Mapstone R: The fellow eye. Br J Ophthalmol 1981;65:410–413.
54.Lowe RF: Acute angle-closure glaucoma. The second eye: an analysis of 200 cases. Br J Ophthalmol 1962;46:641–650.
55.Weiss HS, Shingleton BJ, Goode SM, Bellows AR, Richter CU: Argon laser gonioplasty in the treatment of angle closure glaucoma. Am J Ophthalmol 1992;114:14–18.
56.Carpel EF, Brown JD: Permanent iridoplasty. Am J Ophthalmol 1983;96:113–114.
6
Glaucoma Associated with Raised Episcleral Venous Pressure: The “Red Eye” Glaucomas
Kenneth W. Olander
Definition
How Is Glaucoma from Raised Episcleral Venous Pressure (EVP) Defined?
Increased EVP causing glaucoma may be seen in at least 17 clinical situations (Table 6–1). It is a type of secondary open-angle glaucoma and has four subtypes: (1) obstruction of venous drainage, (2) arteriovenous fistula, (3) ocular episcleral venous anomalies, and (4) idiopathic. This glaucoma is not rare and is commonly underdiagnosed, especially the idiopathic form and those caused by subclinical dural shunts.
Table 6–1. Classification of Elevated Episcleral Venous Pressure (EVP)
I.Venous obstruction
1.Retrobulbar tumors
2.Thyroid ophthalmopathy
3.Superior vena cava syndrome
4.Congestive heart failure
5.Thrombosis of cavernous sinus or orbital vein
6.Vasculitis of the episcleral and/or orbital vein
7.Jugular venous obstruction
8.Inversion therapy
II.Arteriovenous anomalies
9.Carotid-cavernous sinus fistula
10.Orbital varix
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108 Glaucoma Associated with Raised Episcleral Venous Pressure: The “Red Eye“ Glaucomas
Table 6–1 Continued
11.Sturge-Weber syndrome
12.Orbital meningeal shunts (dural shunt syndrome)
13.Carotid jugular venous shunts
14.Orbital vascular shunts
III. Idiopathic causes
15.Sporadic
16.Familial
IV. Medications
17. Oral and topical
Modified from Ritch, Shields, and Krupin, 1996. By permission from C.V. Mosby.
Epidemiology and Importance
How Important and How Common Is Glaucoma from Raised EVP?
This is an important class of glaucoma because it may present at any time to anyone. The recognition of eyes with raised EVP is important for at least three reasons1:
1.The episcleral veins serve as collector channels for the outflow of aqueous from the eye via Schlemm’s canal and the aqueous veins. Thus, a chronic elevation of pressure in the episcleral veins can result in the elevation of intraocular pressure (IOP) with resulting glaucoma and damage.
2.The occurrence of glaucoma secondary to raised EVP dictates that an extensive medical, neurologic, and radiologic evaluation be performed, including arteriography and venography, to determine the cause of the raised EVP.
3.Glaucoma secondary to raised EVP may not respond to some of the medical agents generally used in the treatment of other forms of open-angle glaucoma.
There is no single subspecialty that sees a lot of cases, as this type probably constitutes less than 1% of glaucomas. The patients typically have a red eye, but may not always notice it. Comprehensive ophthalmologists may be the first line of detection of this potentially fatal condition.2 It is almost impossible to define the exact frequency of this disease. As a glaucoma specialist, I had four cases over a 4-year period and then none for many subsequent years. Cornea specialists may see these cases of red eyes and may pick up the elevated IOPs. Neurophthalmologists may see some cases presenting with neurologic defects. Orbital specialists may see patients with pulsating exophthalmos.
A review of the literature indicates a wide range of presenting cases. Keltner et al3 saw 18 cases over 9 years, or two per year. Hieshima et al2 saw 131 cases over 12 years, or 11 per year. Regardless of how many cases are seen, treatment is often challenging and typical medical means do not work. Appropriately diagnosing and treating the underlying cause frequently cures this glaucoma, but often surgical intervention is required.
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Diagnosis and Differential Diagnosis
What Is the Normal Drainage of Aqueous Out of the Eye?
It is necessary to review some basic scientific principles regarding the drainage of aqueous out of the eye and how the vascular plexus and venous pressure cause glaucoma. According to Weinreb and Karwatowski,4 it was Sidel in 1923 who was the first to inject ink into the anterior chamber and observe its appearance in the episcleral veins. They also point out that it was not until 1942 that Ascher observed clear aqueous humor laminated with blood in a vessel demonstrating an anatomic connection between Schlemm’s canal and the episcleral veins. Recent scanning electron microscopy of vascular resin casts has added significantly to our detailed understanding of this anatomy.5 It should be noted that this is a valveless system with frequent interconnections. Indeed, blood can be diverted from one system to the other, with flow in any direction, depending on the hydrostatic pressure gradient.
There is a constant flow of aqueous humor through the anterior segment of the eye. We know that the aqueous is formed by the ciliary processes, passes through the pupil, and exits in the angle. Most of the fluid enters the venous system by way of the trabecular meshwork and Schlemm’s canal; this is called convention outflow. A smaller amount of aqueous passes through the ciliary muscle and the iris to reach the superciliary and superchoroidal spaces. From there, the fluid passes through the sclera or through the loose connective tissue around the penetrating nerves and vessels. This is called unconventional outflow.
What Is Conventional Outflow?
The episcleral tissue is a loose connective and elastic tissue covering the sclera and connecting to the conjunctiva. It is continuous with the loose tissue of Tenon’s space and tightly connects to denser sclera in its deeper layers. It contains multiple blood vessels. Behind the ocular attachments of the recti, the episcleral tissue is thin and the vessels, two veins to each artery, form a wide meshed net. The arteries here come from the posterior ciliary network. In front of the attachment of the muscles, the episclera is much thicker and much richer in vessels. The meshes of the vascular net are smaller. A capillary net exists only in this anterior zone on the sclera. When there is a marked filling of this net, it is called ciliary injection. Aqueous humor drains through the trabecular meshwork into Schlemm’s canal. Arising from the outer circumference of the canal are the external collector channels that drain into the episcleral and conjunctival venous plexus. There are 25 to 35 collector channels. When one of the connects directly with a surface vein, it can be seen on slit-lamp examination and is termed an “aqueous vein.” Some 14 or more branches from the ciliary muscle also traverse the sclera to join the plexus of veins adjacent to the canal. Aqueous veins of Ascher vary in size from 0.01 to 0.1 mm in diameter. They are found near the limbus and most often inferonasally commencing in a hookshaped bend where they come out of the sclera. They contain a clear fluid, and a laminated flow of blood and clear fluid can often be seen.6 Thus, to summarize, the aqueous drains from Schlemm’s canal into a deep scleral plexus of veins, and then via the intrascleral plexus to the episcleral plexus and the subconjunctival plexus at the limbus. In addition, from direct connections, aque-