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Chapter 222 – Angle-Closure Glaucoma

Chapter 222 – Angle-Closure Glaucoma











• Iris apposition or adhesion to the trabecular meshwork, causing a decrease in outflow and an increase in intraocular pressure to clinically significant levels.



• Gonioscopically closed angle.

• Intraocular pressure above the statistical norm.



• Optic nerve atrophy.

• Visual field defects.

• Secondary forms accompanied by a wide array of ocular conditions.

• Pain, redness, mid-dilated pupil when acute.





The many clinical entities grouped under angle-closure glaucoma are characterized by iridotrabecular apposition or adhesion or both. In most cases, no problem is detected until the outflow facility has decreased enough to cause a clinically significant elevation of intraocular pressure (IOP). The sequence of events and the mechanism can be highly variable, however. In each case, an initial attempt to identify the anatomical changes and the pathophysiology must be carried out to make the correct diagnosis and choose the most appropriate management.[1] [2] [3] [4] [5] The principal arguments to separate strictly angle-closure glaucoma from open-angle glaucoma are the primary therapeutic approach (i.e., iridectomy or iridoplasty), the possible late complications (synechial closure of chamber angle), and the complications that result when this type of glaucoma is managed by filtration surgery (uveal effusion, aqueous misdirection glaucoma).

Some confusion and overlap of terminology has arisen in the descriptive terms and definitions of angle-closure glaucoma. Classically, angle-closure glaucoma is subdivided into two main groups according to the cause, known or presumed, of angle closure:

• Primary angle closure, in which no cause other than anatomical predisposition is identified (typical is the classic acute angle-closure attack)

• Secondary angle closure, in which a direct causal relationship is found between iris apposition and a specific condition that arises from pathological processes in any part of the eye. Typical examples are synechial angle closure from contraction of fibrovascular membrane, as in neovascular glaucoma or iridotrabecular apposition from seclusio pupillae with iris bombé in anterior uveitis (see Chapter 225 ).




Risk Favtors for Primary Angle-Closure Glaucoma

Positive family history for angle closure


Age over 40–50 years




History of angle-closure symptoms






Racial group (Eskimo > Asian > Caucasian = African)






Incidence and Prevalence

Compared with primary open-angle glaucoma, few data are available on the incidence and prevalence of the various types of angle-closure glaucoma. The most common form of primary angle-closure glaucoma is associated with some degree of pupillary block or increased resistance to transpupillary flow of aqueous humor. In turn, this results from moderate or firm apposition of the posterior surface of the iris to the anterior surface of the lens, which is associated most often with a narrow anterior segment coupled with the lifelong increase of lens volume. As a consequence, the prevalence of primary angle-closure glaucoma is higher in those with hyperopia, in the elderly patient, in diabetics, in those with pseudoexfoliation, in women, and in certain races ( Box 222-1 ). Iris-induced primary angle closure is not associated specifically with a shallow central anterior chamber (see below).

Risk Factors

Anatomical features characteristic of primary angle-closure glaucoma may be used to identify individual risk. Shallow anterior chamber depth, thicker lens, increased anterior curvature of the lens, smaller corneal diameter, shorter axial length, and increased ratio of lens thickness to axial length are findings agreed upon by independent researchers.[4] [6] Individuals from the groups given in Box 222-1 are at higher risk for the development of primary angle-closure glaucoma. Several studies have shown striking differences by racial group in the distribution of primary angle-closure glaucoma in individuals over 40 years of age, [7] [8] [9] [10] [11] with an incidence in Caucasians of 0.1–0.2%, in Eskimos of 2.2–6.2%, in East Asians of 0.3–3.2%, and in those of mixed race from the Western Cape area of South Africa of 2.3%. Rates increase uniformly with age, and women are affected more often the men, independent of age.

Pathogenesis and Pathophysiology

When the pathogenesis of angle closure is considered, it is critical to analyze each of the following factors:

• Relative and absolute size of anterior segment structures

• Relative and absolute position of anterior segment structures



• Forces involved between the anterior and posterior chambers and their distribution vectors

To better elucidate the several components of angle closure, it is useful to approach the pathophysiology from different standpoints, as given in Box 222-2 .


Pupillary block occurs when a pressure gradient exists between the anterior and posterior iris surfaces, with the pressure in the posterior chamber greater than that in the anterior chamber.

Absolute pupillary block occurs when there is no aqueous flow through the pupil ( Fig. 222-1 ), as in seclusion or occlusion



Pathogenesis and Pathophysiology of AngleClosure



Absolute or relative pupillary block ( Figs. 222-3 and 222-4 )


Forward rotation of ciliary body and/or iris root


Choroidal swelling after panretinal photocoagulation, chronic retinal venous obstruction, posterior scleritis


Anterior insertion of the iris


Anterior position of the ciliary processes


Plateau iris configuration or plateau iris syndrome


Large or anteriorly displaced lens


Aqueous misdirection


Serous or hemorrhagic choroidal detachment or effusion


Space-occupying posterior lesion (gas bubble, synthetic vitreous substitutes, tumor)


Retrolenticular tissue contracture (retinopathy of prematurity, persistent hyperplastic primary vitreous)




Inflammation or hyphema with contraction of fibrin in the angle recess


Neovascularization of the iris with contraction of the fibrovascular membrane


Endothelial proliferation, as in iridocorneoendothelial syndromes


Prolonged anterior chamber shallowing with iridotrabecular contact


Iris incarceration in cataract incision


Epithelial downgrowth


Fibrous ingrowth







Figure 222-1 Absolute pupillary block from seclusio pupillae. The iris bombé is typical, with a normal central anterior chamber depth.



Figure 222-2 Relative pupillary block. View of the iris profile at the slit lamp with a 60° angle.

pupillae, as a result of posterior synechiae (iris to lens, intraocular lens [IOL], capsule, anterior hyaloid). Relative pupillary block occurs when some degree of resistance to forward aqueous flow exists between the surfaces of the anterior capsule and of the posterior iris ( Fig. 222-2 ). Pupillary block also results when an IOL in the anterior chamber of vitreous face blocks the pupil, in the absence of a functioning iridectomy, or from a gas bubble or silicone oil in the anterior chamber. Papillary block needs to be recognized, because it is the most relevant component in the vast majority of cases of angle closure and is managed effectively with laser or surgical iridectomy.


Iridotrabecular apposition or adhesion results from several conditions, alone or in combination. Contraction of fibrovascular and inflammatory membranes in neovascularization of the iris and anterior segment inflammation (uveitis or mechanical irritation from IOL haptics, etc.) may rapidly close an angle synechially. Prolonged anterior chamber shallowing from any cause, such as epithelial downgrowth, fibrous ingrowth, and endothelial proliferation seen in iridocorneoendothelial syndromes, also may result in secondary angle closure.


Lens-induced angle-closure glaucoma has two components—lens size (phacomorphic) and lens position (phakotopic). Lens-induced angle-closure glaucoma results directly when a lens presses against the posterior surface of the iris and ciliary body or indirectly when the increased lens–iris contact hastens the pupillary block component (see Chapter 230 ).


The plateau iris mechanism results from iridotrabecular contact when the pupil is dilated. Also referred to as angle crowding, iris-induced angle-closure glaucoma may occur when any or all of the following occur:

• Tissue of the peripheral iris is thick (peripheral iris roll)

• Iris base inserts anteriorly and leaves only a very narrow ciliary band, or inserts into the scleral spur

• Ciliary processes are displaced anteriorly in the posterior chamber and push the iris base forward into the angle recess[5] ( Fig. 222-3 ).

The relative position of the iris root may be assessed using ultrasound biomicroscopy. The plateau iris mechanism suggests that iris-induced angle-closure glaucoma is not relieved by iridectomy. Angle closure caused by the pure form of plateau iris syndrome is extremely rare, and can be proved only by the occurrence of an acute angle-closure attack triggered by mydriasis despite a patent peripheral iridotomy. A plateau iris configuration, however, is relatively common and frequently coexists with pupillary block.


Primary Acute Angle-Closure Attack

A primary, acute angle-closure attack ( Fig. 222-4 ) may cause symptoms of decreased vision, halos around lights, frontal headache, pain, nausea, and vomiting. Not all of these symptoms



Figure 222-3 Gonioscopic view of an eye that has the lens positioned more anteriorly than usual. The ciliary processes (arrow) are visible through the undilated pupil, a sign of forward rotation of the ciliary body.



are present in all cases and, indeed, little or no complaint may come from the patient.

Signs include an elevated IOP that has risen rapidly, conjunctival congestion, corneal epithelial or stromal edema, Descemet’s folds, shallow or flat peripheral anterior chamber, and a mid-dilated pupil that has an absent or sluggish reaction. Gonioscopy reveals a circumferentially closed angle, and visualization may be poor because of corneal edema. Indentation is important but often technically difficult, because globe firmness and tenderness may result in poor patient cooperation. The fellow eye often shows a narrow, occludable angle or other forms



Figure 222-4 Acute attack of angle-closure glaucoma. The central anterior chamber is deep, intraocular pressure is elevated, and corneal edema is present. Epithelial edema is outlined by the irregular slit reflex (arrow).







Figure 222-5 Typical signs of previous acute or subacute angle-closure attacks. A, Patchy iris atrophy. B, Torsion of the iris. C, Subcapsular, speckled anterior lens opacities (glaucomflecken).

of primary angle closure. In intermittent angle closure (also called subacute angle closure), signs and symptoms are the same as in acute attack, but generally milder, and resolution is spontaneous. The fellow eye has similar gonioscopic findings.

After an acute angle-closure attack, clinical examination may reveal signs of iris torsion ( Fig. 222-5 ), patchy iris sub-atrophy, and lens glaucomflecken. The IOP may be normal or elevated, and the disc shows variable signs of cupping. On gonioscopy, wide areas of appositional or synechial closure (trabecular meshwork not visible in primary position) are found. In the fellow eye, similar synechial closure or a narrow angle occurs.

Chronic Angle-Closure Glaucoma

Few, if any, symptoms are present, unless the IOP is elevated significantly or unless advanced visual field damage is present.[12] Signs include disc cupping or nerve fiber layer defects with or without visual field damage typical of glaucoma, with IOP over 21?mmHg (>2.8?kPa) on no treatment. On gonioscopy, appositional or synechial closure (trabecular meshwork is not visible in the primary position) covers more than 120°. The fellow eye shows a similar gonioscopic picture or narrow angle. Intermittent or chronic angle closure can be deceivingly free of symptoms.

Primary Open-Angle Glaucoma With a Narrow Approach

No symptoms are present unless advanced visual field damage occurs. Signs include an IOP over 21?mmHg (>2.8?kPa) on no treatment, disc or fiber layer defects, with or without visual field damage typical of glaucoma. Gonioscopy reveals an open, but narrow, approach angle (>30°) and frequently a convex peripheral iris surface. The scleral spur often is not visible in the primary position of gaze but becomes visible with dynamic, indentation gonioscopy.

The IOP is increased because of trabecular outflow impairment. When appositional or synechial closure appears as a significant component, the condition is one of angle closure.

Occludable Angle

This is not an objective finding. The fellow eyes of acute angle-closure attack and of chronic angle-closure glaucoma are considered occludable and are managed with prophylactic laser iridotomy.[13] Eyes with extensive appositional closure or peripheral anterior synechia without any apparent cause except for the narrowness of the angle recess are managed as occludable by most clinicians.

Sequence of Events

The sequence of events for the various forms of angle closure are:

• Acute angle closure—sudden, circumferential, iridotrabecular apposition that causes a rapid, severe, and symptomatic rise in IOP

• Intermittent angle closure—self-limiting episodes of iridotrabecular apposition, with milder signs and symptoms than in acute angle closure

• Creeping angle closure—slowly progressive, iridotrabecular contact that results in elevated IOP as soon as 30–65% of the angle is closed

• Chronic angle closure—irreversible, iridotrabecular adhesion that causes asymptomatic IOP elevation

In acute and intermittent angle closure, the iridotrabecular apposition usually is reversed by appropriate intervention; chronic and creeping angle closure are characterized by irreversible peripheral anterior synechiae.

Secondary forms of glaucoma follow the same sequences, but management approaches vary considerably (see Chapters 225 through 230 ).





Gonioscopy (see Chapter 213 ) is used to determine the topography of the anterior chamber angle and is based on the recognition of angle landmarks. In gonioscopy, at least the following must always be considered:

• Level of iris insertion, either true or apparent

• Shape of the peripheral iris profile

• Estimated width of the angle approach

• Degree of trabecular pigmentation

• Areas of iridotrabecular apposition or synechiae ( Fig. 222-6 )

Gonioscopy findings must be recorded using a gradation method. The Spaeth gonioscopy grading system is the only descriptive method to include all the above parameters.[14] Other grading systems, such as the one introduced by Scheie, also are very useful and have become popular. It is not clear which method is better, but a grading system always should be used. Biometric gonioscopy, introduced by Congdon,[15] [16] offers the advantage of a relatively simple and repeatable semiquantitative measurement of the angle, but it is not widely used.

Dynamic indentation gonioscopy is performed in all cases.[17] [18] When pupillary block is the prevalent mechanism, the iris becomes peripherally concave during indentation. In the iris plateau configuration, this concavity does not extend to the extreme periphery, a sign that the ciliary body or iris root is placed anteriorly. When the lens is the cause, the iris moves backward only slightly on indentation and retains a convex profile.

Because patients most commonly have mixed components of angle closure, the cause seldom is clear from gonioscopic appearances.

Dynamic indentation gonioscopy is extremely useful for the differentiation of optical from either appositional or synechial closure and is used to measure the extent of angle closure. Visualization of the ciliary processes through the undilated pupil is a sign of forward displacement of the pupil border and





Figure 222-6 Gonioscopic view of peripheral anterior synechiae. A, Wide-based iridotrabecular adhesions and a relatively wide-angle approach are typical sequelae of inflammation. B, Pointed, tent-like synechiae are often observed in narrow angles with a relative pupillary block.

of the anterior lens surface, and is associated with anterior rotation of the ciliary body (see Fig. 222-3 ).

Slit-Lamp Grading of Peripheral Anterior Chamber Depth

The Van Herick method[19] uses corneal thickness as a unit of measure. Grade 0 represents iridocorneal contact; a space between the iris and corneal endothelium of less than one fourth the corneal thickness is grade I; for grade II the space is between one fourth and one half the corneal thickness; and grade III is considered not occludable, with the iris endothelium distance more than one half the corneal thickness.

Ultrasound Biomicroscopy

Ultrasound biomicroscopy (see Chapter 213 ) of the anterior segment allows accurate visualization of the iris, iris root, corneoscleral junction, ciliary body, and lens.[4] [5] Using this technique, it is possible to elucidate the mechanism of angle closure in almost every patient. However, because of its limited availability and high cost, ultrasound biomicroscopy usually is reserved for those cases most difficult to interpret.

Provocative Tests for Angle-Closure Glaucoma

Overall, provocative tests for angle closure carry some risks and provide limited additional information to that obtained from the clinical examination. [20] [21]


The pupillary block mechanism is increased in mid-dilatation of the pupil and by increased tension of the iris muscle, such as occurs with strong miotic therapy and concomitant dilator muscle stimulation by phenylephrine (Mapstone test). The test is performed using either short-acting parasympatholytic mydriatic agents or phenylephrine eye drops, in association with pilocarpine. The test strategy yields data relevant only to the reaction of a specific eye to a specific agent and is of very limited prognostic value. If the test result proves positive, an acute attack may be triggered. If negative, the test does not rule out angle occlusion under more physiological conditions. Such tests must not be performed simultaneously in both eyes.


The dark room prone test is based on the assumption that the pupil dilates in the dark and the lens moves slightly forward in the prone position. The test is conducted as follows. The patient sits for at least 30 minutes in the dark with the head pronated, usually resting on a table, and must not be allowed to fall to sleep, because sleep can cause pupil constriction. The IOP is checked rapidly, with the room light still off. The test result is considered positive when the IOP increases by 8?mmHg (1.1?kPa) or more or gonioscopy shows unquestionable increase of the areas that have appositional closure. The mechanism is unclear but may be related to mydriasis and the forward movement of the lens. The results apply only to the specific conditions of the test—its value in the prediction of actual behavior is not known.


Iris Bombé or Anterior Pupillary Block

The flow of aqueous through the pupil is hindered by adhesions that occur between the pupillary margin and the anterior lens surface. This block can be relative or absolute, as in seclusion pupillae or in occlusion pupillae. Although aqueous accumulates between the lens and iris to cause the iris to balloon forward, little or no anterior displacement of the lens occurs. The clinical picture of iris bombé, with the anterior chamber shallow peripherally but deep centrally, is typical. In pseudophakic eyes this type of block to aqueous flow is observed when posterior synechiae develop between the iris and the IOL at the pupillary border. Management of the cause is effected by creating a laser iridotomy or surgical iridectomy.



Posterior Pupillary Block or Anterior Aqueous Misdirection


In phakic eyes, the flow of aqueous toward the pupil is made difficult, because the posterior iris surface is wrapped tightly around the lens. The iris–lens contact is aggravated by aqueous that accumulates around and behind the crystalline lens; the aqueous pushes the lens forward with the iris and worsens the difficulties in forward aqueous flow. Phacomorphic or lens-position glaucoma, as well as the classic primary angle-closure attack, are typical.[22] The clinical picture is characterized by a shallow central anterior chamber. It is conceivable that aqueous pressure builds up in the small space between the zonulocapsular plane and the periphery of the anterior hyaloid face, which is referred to anatomically as the canal of Petit. Management includes iridectomy or lens extraction or both. Miotic agents may worsen the transpupillary aqueous flow difficulties.


After extracapsular cataract extraction or phacoemulsification, with or without posterior chamber IOL implantation, when aqueous accumulates behind the iridocapsular diaphragm the posterior lens capsule and IOL, if present, are pushed forward.[22] The clinical picture is characterized by a shallow central anterior chamber. The space between the capsule and anterior hyaloid, in which the aqueous accumulates, becomes exaggerated and may be detected by biomicroscopy. Management requires the re-establishment of communication between the posterior and anterior chambers by performing a capsulectomy or iridectomy. Miotic medications have no role and may worsen the aqueous flow difficulties.

Posterior Aqueous Misdirection or Malignant Glaucoma

In this disorder, the aqueous humor is misdirected posteriorly and accumulates within the vitreous cavity, either diffusely or in the form of lacunae. The volume increase of the vitreous body displaces the lens or IOL anteriorly. The clinical picture is characterized by the anterior chamber becoming more shallow, both centrally and in the periphery. Classically, this condition is known as malignant glaucoma. Ciliary block glaucoma is described by some authors as a separate entity, in which aqueous accumulates behind a layer of condensed anterior vitreous. The change in aqueous dynamics may be spontaneous, although commonly it is propagated by a wound leak, whether unintentional or deliberate (as in filtration surgery). [22] Management entails the re-establishment of communication between the posterior chamber and the anterior chamber. Aqueous suppressant, osmotic, mydriatic, and cycloplegic agents are employed before laser capsulectomy (in pseudophakes), iridectomy, laser vitreolysis, or pars plana vitrectomy is attempted. Lens or IOL removal is seldom necessary. Miotic medications have no role and may worsen the aqueous flow difficulties.


Pharmacological Mydriasis

Dilatation of the pupil using topical or systemic drugs may trigger iridotrabecular contact and eventually result in angle closure. Angle-closure attacks may occur, even bilaterally, in patients treated with systemic parasympatholytic agents before, during, or after abdominal surgery, and have been reported in association with the use of a serotoninergic appetite suppressant.[23]

Although pharmacological mydriasis using topical tropicamide and phenylephrine is safe in the general population,[24] [25] even in eyes that have very narrow approach, a raised IOP and angle occlusion may occur in the occasional patient.[26]

Theoretically, any psychoactive drugs have the potential to cause angle closure; it is unlikely that pretreatment gonioscopy findings alone help to rule out such a risk. In eyes that have narrow angles, gonioscopy and tonometry are repeated after the initiation of management. Prophylactic laser iridotomy needs to be evaluated against the risks of angle closure or of withdrawal of the systemic treatment.

None of these drugs is contraindicated per se in open-angle glaucoma.

Ciliochoroidal detachment in association with bilateral angle closure has been reported after the administration of oral sulfa drugs,[27] and also in patients with acquired immunodeficiency syndrome, according to at least two reports.[28]


Primary Angle-Closure Attack

Primary angle-closure attack is an ophthalmologic emergency, in which the priorities are ( Fig. 222-7 ):

• Break the attack

• Lower the IOP

• Safeguard the fellow eye[29]



Figure 222-7 Initial management of primary, acute angle-closure attack.



Topical pilocarpine 2% or dapiprazole administered twice in 5 minutes, a topical ß-blocker, a topical a2 -agonist, and a topical corticosteroid are given immediately, along with an osmotic agent at full dose or intravenous acetazolamide 5–10?mg/kg.

Corneal indentation using a blunt instrument is best performed using a Zeiss-type four-mirror gonioprism, which may force aqueous through the pupil by misalignment of the iris sphincter or open an area of appositionally closed trabecular meshwork and, thus, allow aqueous to exit the anterior chamber.[30] A lower IOP achieved by these means decreases iris ischemia and enables pilocarpine to constrict the pupil effectively.

The patient must lie supine, to allow the lens to fall back into position. If vomiting occurs, intramuscular metoclopramide can be given. If significant pain occurs, topical ketorolac tromethamine and systemic pain medication may be given.

The patient is re-evaluated within 60–90 minutes. If the eye is quite comfortable, a prophylactic iridectomy is performed in the fellow eye. If the pupil is constricted and the IOP lowered, topical corticosteroid four times a day, pilocarpine 2% three times a day, a ß-blocker twice a day, and an a2 -agonist are prescribed, and a topical or oral carbonic anhydrase inhibitor is considered. Depending on corneal clarity and inflammation, laser iridectomy may be performed immediately or may be scheduled.

If the pupil does not respond and the IOP remains elevated, yet the cornea is sufficiently clear, a laser iridectomy may be attempted. Peripheral or radial argon laser iridoplasty may be performed even through a cloudy cornea; this procedure may break an acute attack and allow subsequent laser iridectomy. Peripheral clear cornea paracentesis has been suggested as a possible way to break the attack. [31]

Only in the rare cases in which the attack cannot be broken is emergency surgery considered. If pupillary block is the main problem, peripheral iridectomy is the procedure of choice. Cataract extraction ideally is not performed in an inflamed eye that has a hazy cornea and is considered only when the lens is the major cause of angle closure. Ultrasound biomicroscopy may be very helpful for cases that do not respond to initial medical or laser management.

For primary angle-closure glaucoma the use of miotic drugs is widespread. However, parasympathomimetic agents may worsen the pupillary block and cause forward movement and anteroposterior thickening of the lens. Pilocarpine is not effective if the iris sphincter is ischemic, such as when IOP is over 50?mmHg (>6.7?kPa).

The long-term use of miotic agents generally cannot prevent acute or chronic angle-closure glaucoma and should not replace prophylactic iridotomy or iridectomy. In cases of combined pupillary block and plateau iris, iridectomy is performed first. Plateau iris may be managed using argon laser iridoplasty or miotic therapy or both, preferably with sympatholytic agents such as dapiprazole or thymoxamine—strong miotic medications are avoided, because anterior rotation of the ciliary body occurs when the ciliary muscle is stimulated pharmacologically. Once the angle closure episode is managed successfully, a dilated examination is indicated. This is essential to rule out posterior segment abnormalities as a primary cause of the angle closure, to assess optic nerve damage, to evaluate the lens, and to break early posterior synechiae.

Management options for the secondary forms of angle-closure glaucoma and malignant glaucoma are given in Chapters 225 through 227 , 229 , and 230 .

Management Principles

In general, plateau iris is managed by iridoplasty, pupillary block by iridectomy or iridotomy, and lens-induced glaucoma by lens extraction.


The main indications for peripheral iridoplasty ( Fig. 222-8 ) are:[32] [33] [34] [35] [36] [37]





Figure 222-8 Angle-closure glaucoma with pupillary block component. A, No angle structures are visible in the primary position. B, After iridectomy, the iris curvature is less pronounced, and the trabecular meshwork can be visualized.

• Plateau iris (syndrome or configuration), for which argon laser iridoplasty is the management of choice if iridectomy fails to widen the angle

• Acute attacks when corneal edema precludes laser iridotomy and medical management fails to break the attack (radial iridoplasty also is indicated)

• Primary open-angle glaucoma, before argon laser trabeculoplasty (ALT), when the angle approach is too narrow to visualize the trabecular meshwork


The therapeutic goal is to shrink and flatten the iris tissue with no resultant perforation, bubble formation, or pigment dispersion—excessive intervention may cause necrosis.[38] For peripheral iridoplasty, the laser is aimed at the extreme periphery of the iris, and a single row of evenly spaced applications made, 5–12 per quadrant at no less than one-spot–diameter intervals (see Fig. 222-8 ). Radial iridoplasty may be used to dilate the pupil and break a pupillary block, and is performed by the application of double rows of low-power, 200–500?µm diameter laser spots radially on the oblique meridians, from near the pupil margin to the periphery, starting superiorly.

The technique and settings for laser iridectomy and iridoplasty are discussed in more detail in Chapter 235 . See also below under Occludable Angle.


Iridectomy is the removal of iris tissue by a knife and scissors (surgical iridectomy) or by different forms of lasers, which remove iris tissue by dissolution (so-called laser iridotomy). Iridotomy, although rarely used today, is an opening in the iris without removal of iris tissue, usually performed by means of a knife needle perforating the iris.

Since the advent of laser iridectomy, surgical peripheral iridectomy is no longer performed commonly, but it is important to know how to perform the operation safely for the rare occasions on which it is needed. After preoperative medical therapy, which includes osmotic agents, to lower IOP, a 2–3?mm incision is made in the peripheral cornea in a superior quadrant (usually superotemporally). Alternatively, a small conjunctival peritomy is made and the incision placed at the scleral limbus. The initial incision is to about two thirds of the corneal thickness, and a nylon suture is placed and looped out of the incision groove. An assistant may use this suture to open or close the incision later and thus control the rate of egress of aqueous. Care must be taken when the anterior chamber is entered with the blade and,



after the initial penetration, an upwardly directed cut is advisable to extend the deep opening.

The key to success is to make the incision vertical so that a knuckle of iris spontaneously engages into the wound. Counterpressure on the back lip of the incision may encourage iris prolapse. This externalized piece of iris is held with toothed forceps and incised using fine scissors. If at all possible, neither the toothed forceps nor the scissors is used to enter the anterior chamber in an attempt to grab and cut the peripheral iris, because the lens and other underlying structures may be damaged. The edges of the incision are stroked gently to encourage the cut iris ends to retract into the anterior chamber, and the corneal or scleral incision is closed with one or two 10-0 nylon sutures to achieve a watertight closure.


Peripheral anterior synechiae sometimes may be stripped from the angle wall using an irrigation cyclodialysis spatula or flat iris spatula.[39] [40] The procedure requires anterior chamber deepening with viscoelastics and restores trabecular function only if adhesions have been present for less than 1 year.


In primary angle-closure glaucoma, filtration surgery is more prone to both intraoperative and postoperative complications, such as intraoperative positive pressure, zonular or lens damage, aqueous misdirection, and choroidal effusion or hemorrhage. It is important for the trabeculectomy scleral flap to be placed well anteriorly (see Chapter 240 ).


The removal of a lens that has early opacities, or even of a clear lens, is suggested by some clinicians as the management of choice for angle-closure glaucoma induced mainly by lens size or malposition (see Chapter 229 ). That lens opacities possibly worsen rapidly, as occasionally observed after filtration surgery, lends further support to this approach. Excellent anatomical and functional outcomes are routine with modern closed-system, small-incision phacoemulsification. [31] [41] [42] [43] [44] Angle-closure cases may be very challenging, however, because of a small pupil, posterior synechiae, shallow anterior chamber, lax zonules, positive pressure, and lowered endothelial cell counts after acute angle-closure attacks.[45] [46] [47]


Laser iridectomy, laser iridoplasty, and cataract extraction are applied sequentially. The same drugs as used in primary open-angle glaucoma (POAG) are prescribed, because long-term miotic therapy does not prevent and actually may hasten progressive angle closure.


Laser iridectomy is the management of choice for an occludable angle. If iridectomy fails to widen the angle, iridoplasty is considered. The reported rate of occurrence of primary, acute angle-closure attacks in such patients who are not treated is in the range 7–37%.[48] The discrepancy is probably because of different diagnostic definitions of occludable angles. Once the diagnosis is made, the risks of receiving or not receiving treatment need to be discussed with each patient. The major long-term drawback of laser iridectomy or iridoplasty is the formation of posterior synechia that can hinder mydriasis and make subsequent cataract surgery more difficult


Medical management is given initially, as for other patients who have POAG. Gonioscopy is repeated regularly. Although ALT is as effective as in POAG, it may need to be associated with argon laser iridoplasty to allow proper visualization of the trabecular meshwork.


Gonioscopy and ultrasound biomicroscopy help to direct the management. When the trabecular meshwork is visible, ALT may be performed. With appositional closure, iridoplasty is applied before ALT. Synechial closure requires filtration surgery.

In lens-induced attacks, laser iridectomy or iridoplasty may be used successfully to open the angle and lower the IOP, and thus allow the scheduled lens extraction to be carried out on a less inflamed eye with a clearer cornea.

Iridectomy Failure

The failure of iridectomy to cure pupillary block may result from two conditions—the iridectomy is too small (functional failure) or it is closed (anatomical failure).[49]

Functional failure is rare and theoretically may be prevented if the iridectomies will remain of an adequate size. Hydrodynamically speaking, a 30?m diameter opening should suffice to eliminate the pressure gradient between anterior and posterior chambers. The size of an iridectomy, however, may decrease shortly after surgery because of the elastic recoil of the stroma or localized edema. A minimal diameter of 50–100?m is required. Occasionally, in secondary angle closures, loculation of the iris bombé may occur, and more than one patent iridectomy may be required to relieve the condition.

Anatomical closure may occur after the closure of an initially patent iridectomy and is more common after argon laser than neodymium:yttrium-aluminum-garnet laser iridotomy or in certain conditions such as uveitic or neovascular glaucoma. It is important to ensure that the iridectomy is full thickness at the outset, with penetration of the posterior pigmented iris layer (see Chapter 235 ).


The medical and laser surgical treatments of acute primary angle-closure glaucoma have a high success rate, especially if the disease is diagnosed early. It is important to manage prophylactically (with iridectomy) the fellow eye of patients who have angle-closure glaucoma with a pupillary block component, because a high incidence exists of future attack in this eye and the risk–benefit ratio greatly favors such prophylactic therapy. Blood relatives and siblings of patients show higher risk for primary angle closure.[14] [50] Patients who have secondary angle closures follow a course that often is dependent upon their underlying disease. For example, in patients with neovascular glaucoma, the underlying retinopathy from chronic retinal venous obstruction or diabetes may affect visual outcome profoundly.

Interestingly, in a Caucasian population the probability of monocular blindness in acute primary angle-closure glaucoma was found to be 14% at the time of diagnosis, and among those non-monocularly blind at diagnosis, a further 4% will be so in 5 years. Such incidence data indicate the need for early diagnosis and appropriate treatment.[7]





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37. Lam DS, Lai JS, Tham CC, et al. Argon laser peripheral iridoplasty versus conventional systemic medical therapy in treatment of acute primary angle-closure glaucoma: a prospective, randomized, controlled trial. Ophthalmology. 2002;109(9): 1591–6.


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48. Panek WC, Christensen RE, Lee DA, et al. Biometric variables in patients with occludable anterior chamber angles. Am J Ophthalmol. 1990;2:185–8.


49. Gross FJ, Tingey D, Epstein DL. Increased prevalence of occludable angles and angle-closure glaucoma in patients with pseudoexfoliation. Am J Ophthalmol. 1994;117:333–6.


50. Tomlinson A, Leighton D. Ocular dimensions in the heredity of angle-closure glaucoma. Br J Ophthalmol. 1973;57:475.


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