nificant pain, elevated IOP, and a shallow anterior chamber in the periphery. The eye tends to be more inflamed than with serous choroidal detachments and the dome-shaped elevation is dark red by ophthalmoscopy. β-scan can also be used to confirm the diagnosis.

In addition, processes that push the lens and iris anteriorly can cause an acute or subacute IOP elevation with a shallow anterior chamber. Thus, a careful search should be made for spaceoccupying lesions such as tumors or cysts of the iris, ciliary body or retina, or even massive subretinal hemorrhage. Transudation of fluid after a CRVO can hydrate the vitreous, leading to anterior movement of the lens-iris diaphragm and resultant peripheral and central shallowing of the anterior chamber, mimicking malignant glaucoma.

TREATMENT

Systemic/local

For many years, miotic therapy was used to treat malignant glaucoma. It was found to be unsuccessful and in fact may worsen or precipitate the attack. The first reported success of medical therapy came in 1962 with the use of mydriaticcycloplegic drops. Mydriatic-cycloplegic drops now form a crucial part of the medical management of malignant glaucoma, with the concurrent use of topical aqueous humor suppressants, oral carbonic anhydrase inhibitors, and hyperosmotics. This combination may be tried for 4 to 5 days and is successful in approximately 50% of cases. If medical therapy fails, then surgical intervention is indicated.

real time images of anterior segment structures, allowing for identification of irido-corneal touch, appositional angle closure, anterior rotation of the ciliary body, and ciliary body-iris. The system uses 50to 100-MHz transducers that are incorporated into a β-mode clinical scanner. Higher frequency transducers are used for fine resolution of superficial structures, whereas lower-frequency transducers are used for increased depth of penetration. Resolution ranges from 20 to 60 microns, with tissue penetration approximately to a depth of approximately 4 mm.

UBM studies have allowed identification of a subset of patients with malignant glaucoma in whom the pathologic mechanism is due to annular ciliary body detachment rather than aqueous misdirection. Liebmann and colleagues found the presence of fluid accumulation limited to the supraciliary space, which was detectable only by UBM. Drainage of the supraciliary fluid with reformation of the anterior chamber resulted in normal ocular anatomy and IOP.

REFERENCES

Chandler PA, Grant WM: Mydriatic-cycloplegic treatment in malignant glaucoma. Arch Ophthalmol 68:353, 1962.

Greenfield DS, et al: Aqueous misdirection after glaucoma drainage device implantation. Ophthalmology 106:1035–1040, 1999.

Quigley HA, Friedman DS, Congdon NG: Possible mechanisms of primary angle-closure and malignant glaucoma. J Glaucoma 12:167–180, 2003.

Ruben S, Tsai J, Hitchings R: Malignant glaucoma and its management. Br J Ophthalmol 81:163–167, 1997.

Weiss DI, Shaffer RN: Ciliary block (malignant) glaucoma. Trans Am Acad Ophthalmol Otolaryngol 76:450, 1972.

Surgical

Surgical intervention consists of argon laser treatment of ciliary processes, Nd : YAG laser hyaloidotomy, and incisional surgery. The key to surgical intervention lies in creating a channel of communication between the vitreous cavity and the anterior chamber, allowing for normalization of pressures between the two chambers.

Herschler first reported the use of argon laser to shrink ciliary processes via the peripheral iridectomy to treat malignant glaucoma. Successful treatment required shrinkage of 2 to 4 processes. Nd : YAG laser hyaloidotomy has also been described to be successful in treating pseudophakic and aphakic malignant glaucoma. The procedure involves photodisruption of the lens capsule and the anterior vitreous face.

For cases in which medical and laser therapy fail, pars plana vitrectomy is warranted. In the phakic patient, lensectomy at the time of vitrectomy may be considered when there is marked corneal edema, dense cataract, or when the anterior chamber

269 NORMAL-TENSION GLAUCOMA (LOW-TENSION GLAUCOMA)

365.12

Teresa C. Chen, MD

Boston, Massachusetts

Normal-tension glaucoma (NTG) is a progressive optic neuropathy characterized by retinal nerve fiber layer thinning, optic nerve head cupping, and visual field defects. Clinical signs are similar to those found in patients with chronic open angle glaucoma, but documented intraocular pressures are within the statistically normal range. In order to make a diagnosis of

TREATMENT

Until other risk factors for field progression are elucidated, the mainstay of NTG treatment is similar to that for chronic open angle glaucoma and is the lowering of intraocular pressure.

Ocular

Many neuroprotective agents are designed to help improve optic nerve blood flow and function. Some potentially useful medications include calcium channel blockers (e.g. nifedipine, nimodipine), serotonin antagonists, betaxolol, dorzolamide, brimonidine, and memantine. The specific use of these agents for optic nerve blood flow improvement or for neuroprotection should not be practiced until their benefits are more definitively shown in humans.

Medical

All of the major classes of glaucoma medications have been used to treat NTG (i.e. beta blockers, alpha adrenergic agonists, carbonic anhydrase inhibitors, prostaglandin analogues and miotics).

Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normaltension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol 126(4):487–497, 1998.

Collaborative Normal-Tension Glaucoma Study Group. The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma. Am J Ophthalmol 126(4):498–505, 1998.

Drance S, Anderson DR, Schulzer M: Risk factors for progression of visual field abnormalities in normal-tension glaucoma. Am J Ophthalmol 131:699–708, 2001.

Sarfarazi M, Child A, Stoilova D, et al: Localization of the fourth locus (GLC1E) for adult-onset primary open-angle glaucoma to the 10p15-p14 region. Am J Hum Genet 62(3):641–652, 1998.

270 OCULAR HYPERTENSION 365.04

Adam C. Reynolds, MD

Oklahoma City, Oklahoma

Surgical

Available surgical treatments include argon laser trabeculoplasty, selective laser trabeculoplasty, trabeculectomy with or without antimetabolites (i.e. mitomycin C and 5-fluorouracil), tube shunt surgery, and cyclodestructive procedures.

COMMENTS

The Collaborative Normal Tension Glaucoma Study is the first national, multi-center, prospective, randomized study to prove that lowering of intraocular pressure slows down glaucomatous progression in NTG. It also emphasized that a significant proportion of NTG patients still exhibit disease progression despite lowering of intraocular pressure. This underscores the need for further research on the pressure-independent causes of NTG, which may ultimately yield better treatment strategies in the future. As new genes associated with NTG are found, this may also provide another distant venue for treatment in these patients.

SUPPORT GROUPS

Glaucoma Support Network Glaucoma Research Foundation 490 Post Street

Suite 830

San Francisco, CA 94102 (415) 986-3162

Toll free: 800-826-6693 Fax: 415-986-3763

Glaucoma Research Foundation: http://www.glaucoma.org/living/support_ net.html

INTERNET RESOURCES

American Academy of Ophthalmology: http://www.aao.org

ETIOLOGY/INCIDENCE

Ocular hypertension is elevated intraocular pressure (IOP) without any evidence of glaucomatous optic neuropathy. It is not a disease; however, increased eye pressure is the most important risk factor in the development of open angle glaucoma. Ocular hypertension can be categorized similarly to glaucoma with various possible mechanisms of etiology associated with an open or closed (or narrow) angle and associated primary or secondary causes. This chapter will deal with primary ocular hypertension, a condition similar to primary open-angle glaucoma (POAG).

Ocular hypertension has been defined as a mean intraocular pressure greater than 21 mmHg. Based on several different population studies, two standard deviations above mean IOP of 15–17 mmHg occurs at a cutoff of approximately 22 mmHg. In populations of European descent, primary ocular hypertension has been reported in approximately 5% of persons aged 50 years and older. In the United States this translates to approximately 3.9 million individuals. However, ocular hypertension in the United States is more common in individuals of African descent. Several very well-known studies show the exponential rise in the incidence of glaucoma in individuals with IOPs in the 25 mmHg range, particularly in African Americans.

It is important to recognize, however, that ocular hypertension is only one of many factors contributing to the development of glaucomatous optic neuropathy and associated vision loss. Patients with ocular hypertension belong to the much larger group of patients at risk for glaucoma, including those with atypical or asymmetrical optic discs or strong family histories of glaucoma. The Ocular Hypertension Treatment Study (OHTS) has provided a great deal of new information on the risk of glaucoma development from ocular hypertension and the impact of treating ocular hypertension on glaucoma.

●Ciliary body tumors.

●Postradiation treatment.

●Intraocular copper foreign bodies.

Vascular

●Carotid vascular disease or occlusion of other tributaries to the ciliary body (ophthalmic artery and long posterior ciliary arteries) resulting in ocular ischemia.

●Temporal arteritis.

approach that begins with conservative treatments (steroids, mydriatics), followed by argon laser photocoagulation of the cyclodialysis cleft, and finally surgical repair. More information, including surgical techniques, is available from previous manuscripts (see References below).

Early postoperative hypotony occurs commonly with glaucoma filtration surgery. In most cases, hypotonous changes resolve spontaneously over two to four weeks with conservative treatment. In the meantime, patience and vigilance are required

nists, clonidine).

●Hemifacial atrophy.

Increased facility of outflow

Surgical

●Corneal, scleral, or conjunctival wound leak after intraocular surgery.

●Glaucoma surgery.

in hypotony in a monkey model. In addition, the eye may develop reccurrence of ciliochoroidal effusions after surgical drainage and may require further surgery, especially when inflamed. In summary, most hypotonous eyes do not usually require treatment in the early postoperative period after glaucoma surgery, but when required, drainage of ciliochoroidal effusions is essential.

Late postoperative hypotony, 6 months or more after glau-

Traumatic

●Cyclodialysis cleft (also after complicated intraocular surgery).

●Topical cholinergic medications (pilocarpine, carbachol, echothiophate, etc.) may open a previously closed cyclodialysis cleft.

●Ruptured globe.

Uveitis may create increased uveal scleral outflow.

Retinal abnormalities

●Rhegmatogenous retinal detachment.

●Retinal tears and retinotomies.

TREATMENT

The most important factor in treating ocular hypotony is diagnosing the primary cause of the low intraocular pressure. We describe the common treatments below, but clinicians will need to employ specific treatments for each primary cause of hypotony.

Conservative treatments include the use of corticosteroids and topical cycloplegic agents, and avoiding medications that augment hypotony. Corticosteroids help improve ciliary body function by decreasing inflammation that may cause decreased aqueous production and increased uveal scleral outflow. They may be given orally, topically, or locally. Topical cycloplegic eye drops relax the lens, iris, and ciliary body, decreasing the potential space for subciliary effusions. These drops may allow small cyclodialysis clefts to close, as well as reduce inflammation by increasing the blood-brain barrier. Clinicians should limit

Conservative treatments may resolve the hypotony in a minority of cases, but these eyes usually require a bleb revision. In a bleb revision, a surgeon will remove the avascular, necrotic conjunctival tissue and replace it with healthy conjunctiva. This will resolve the hypotony in the majority of cases. A recent study by Bashford has shown that the length of time of hypotony maculopathy is not related to improvement in visual acuity, and most patients will recover good visual acuity even after a long period (6 months or more) of hypotony. This suggests that the surgeon can delay bleb revision until all conservative treatments have failed.

The clinician must anticipate that successful treatment of hypotony may result in severely elevated intraocular pressure. This usually occurs with the normalization of aqueous production and a short-term decrease in trabecular outflow. The clinician should warn the patient of the symptoms of ocular hypertension and should evaluate the patient soon after treatment and at regular intervals. Clinicians should use topical aqueous suppressant glaucoma medications to treat the ocular hypertension until physiologic trabecular outflow returns.

COMMENTS

Clinicians consider an eye to be hypotonous when low intraocular pressure (IOP) results in anatomical or functional abnormalities to the eye. Treatment of hypotony requires an extensive history and complete ophthalmic examination. An accurate diagnosis is the cornerstone to treatment. While selected cases of ocular hypotony may resolve with conservative treatment, some eyes may require surgical intervention when the benefits outweigh the risks of the surgery.

REFERENCES

Barasch K, Galin MA, Baras I: Postcyclodialysis hypotony. Am J Ophthalmol 68:644–645, 1969.

Brubaker RF, Pederson JE: Ciliochoroidal detachment. Surv Ophthalmol 27:281–289, 1983.

Maumenee AE, Stark WJ: Management of persistent hypotony after planned or inadvertent cyclodialysis. Am J Ophthalmol 71:320–327, 1971.

Ormerod LD, Baerveldt G, Sunalp MA, Riekhof FT: Management of the hypotonous cyclodialysis cleft. Ophthalmology 98:1384–1393, 1991.

Pederson JE, Gaasterland DE, MacLellan HM: Experimental ciliochoroidal detachment: Effect on intraocular pressure and aqueous humor flow. Arch Ophthalmol 97:536–541, 1979.

In the United States, 2.2 million persons have been diagnosed with OAG, and it is estimated that at least another 2 million persons have undiagnosed OAG. Among Americans, it is the third most common cause of blindness in the United States, and in blacks of African ancestry, it is the leading cause of blindness. In the United States, with more than 3 million office visits per year related to OAG, it is not only a major ocular but also a major public health and economic problem. Worldwide, it is estimated that 65 million people have glaucoma and 5 million are blind from the disease.

272 OPEN-ANGLE GLAUCOMA 365.10

Emily Patterson, MD

Portland, Oregon

ETIOLOGY/INCIDENCE

Open-angle glaucoma (OAG) is a chronic bilateral ocular disease characterized by optic nerve damage manifested in morphologic and psychophysical changes. The anterior chamber angle is open, and there are no known ocular or systemic causes for the optic nerve damage. The morphologic changes include progressive loss of optic nerve fibers, optic nerve cupping, and thinning of the optic nerve rim, as noted on ophthalmic examination. The psychophysical changes include visual field (VF) defects such as nasal steps, arcuate scotomata, paracentral scotomata, and generalized depression.

The traditional triad on which the diagnosis of OAG was based included optic nerve changes, VF defects, and elevated intraocular pressure (IOP) to least 21 mmHg. However, it has become abundantly clear that a significant portion (approximately 30%) of patients with typical optic nerve or VF changes never have elevated IOP, whereas a similar proportion of patients with OAG continue to have progressive optic nerve and VF changes despite a lowering of the IOP to a ‘normal’ level.

The current concept of OAG is that it is a progressive optic neuropathy with elevated IOP as a major, but certainly not the only, risk factor. Furthermore, it is a multifactorial and heterogeneous disease whose diagnosis is really made by exclusion. Many cases historically been included under the rubric ‘primary’ OAG have been shown with advancing knowledge and diagnostic tools to be secondary glaucomas, such as pigmentary glaucoma and pseudoexfoliation glaucoma.

The cause of OAG remains unknown, but many risk factors have been identified. Elevated IOP is a major risk factor, with higher IOPs associated with greater risk and greater severity of optic nerve damage even in the normal-pressure OAG group. Other risk factors documented in various clinical trials include large optic nerve cup, thin central cornea, high myopia, older age, positive family history, African or Latino ancestry, diabetes mellitus, systemic hypertension, and history of migraine headaches.

The genes for several types of secondary OAG and subsets of juvenileand adult-onset OAG have been identified, and it is almost certain that other genes for this heterogeneous disease will be identified soon.

COURSE/PROGNOSIS

OAG is a chronic disease for which there is no cure-only control. Until the end stages of the disease, when VF loss encroaches on visual fixation, there are no symptoms to warn the patient. Because it is considered unethical to withhold treatment from a patient with OAG, the natural history of the untreated disease is poorly documented. Not all risk factors for this disease have been identified, much less quantified. To further confound the elucidation of its natural history, there is a normal attrition of all nerve cells with age, including the nerve cells in the optic nerve.

Available studies show that 4% of white patients and 8% of black patients with OAG are legally blind due to this disease. Controlled studies of patients at high risk for glaucoma suggest that medical treatment may decrease the risk of developing glaucoma by 50%. The incidence of debilitating visual loss from OAG is low and treatment can significantly improve disease prognosis. However, because of the large number of people afflicted with this disease, the magnitude of the effect of this disease is still substantial.

DIAGNOSIS

Clinical signs

Intraocular pressure

●As many as 30% of patients have ‘normal’ IOP (less than 21 mmHg) at all times

●As many as 50% have ‘normal’ IOP at any single IOP measurement.

●IOP of at least 21 mmHg should arouse suspicion of OAG; the higher the IOP, the greater the likelihood of OAG.

●Asymmetry of IOP with difference between eyes greater than several millimeters of mercury is also suspicious.

Optic nerve

●Size of optic nerve cupping: there is a wide variation in the normal optic nerve cup size, but cups of more than 50% are suspicious. The larger the cup, the more suspicious.

●Asymmetry of optic nerve cupping: physiologic optic cups may be large, but the two eyes should be symmetric. An asymmetry of more than 10% is suspicious; the greater the asymmetry, the greater the likelihood of OAG. Asymmetric cupping associated with ipsilateral higher IOP is even more suspicious.

●Shape of optic nerve cup: physiologic cupping tends to be round with an intact, even rim of nerve tissue. Glaucomatous nerve cupping tends to be uneven with more vertical cupping toward the inferotemporal and superotemporal

Sympathomimetic agonists

Nonselective (a1 and a2)

●Epinephrine bitartrate 2% b.i.d. to q.i.d.

●Epinephrine borate 0.5%, 1%, or 2% b.i.d. to q.i.d.

●Epinephryl borate 0.5%, 1% b.i.d. to q.i.d.

●Epinephrine hydrochloride 0.5%, 1%, or 2% b.i.d. to q.i.d.

●Dipivefrin hydrochloride 0.1% (a prodrug of epinephrine) b.i.d. to q.i.d.

Selective a2

●Apraclonidine 0.5%, or 1% b.i.d. or t.i.d.

●Brimonidine 0.2% b.i.d. or t.i.d.

IOP is decreased 25% by decreasing aqueous production and increasing uveoscleral outflow.

Side effects:

●Cardiovascular: systemic hypertension, tachycardia, arrhythmia with nonselective agents;

Carbonic anhydrase inhibitors

Systemic

●Acetazolamide 125, 250, and 500 mg time release b.i.d. to q.i.d.

●Dichlorphenamide 50 mg b.i.d. to q.i.d.

●Methazolamide 25 and 50 mg b.i.d to t.i.d.

Side effects:

●Gastrointestinal: nausea, vomiting, anorexia, metallic taste;

●Genitourinary: urinary frequency, kidney stones, acidosis;

●Central nervous system: malaise, depression, loss of libido, numbness and parathesia of extremities;

●Hematologic: aplastic anemia, thrombocytopenia (rare);

●Allergic: because all carbonic anhydrase inhibitors are sulfonamide derivatives, they should be used with caution in persons with a history of allergy to sulfur compounds.

dine, intermediate with others;

●Cystoid macular edema: in aphakic or pseudophakic eyes with open capsule with nonselective agents;

●Oral dryness with brimonidine;

●Central nervous system: fatigue, drowsiness with brimonidine.

Because of the high incidence of side effects and because they are minimally additive to the ß-blockers, most of the nonselective sympathomimetic agents are used infrequently. The addition of an epinephrine compound to a selective β-blocker is comparable in magnitude of IOP lowering to a nonselective

β-blocker alone. Apraclonidine is useful in blunting the IOP spikes after laser procedures, but it is not effective in eyes already on treatment with this medication. In addition, the efficacy of apraclonidine decreases with chronic use. Brimoni-

dine may be used as an alternative first-line medication when β-blockers are contraindicated.

Prostaglandin analogs

●Latanoprost 0.005% qd.

●Travoprost 0.004% qd.

●Bimatoprost 0.03%.

●Prostaglandin F2a analogs.

●Decrease IOP 25% to 30% by increasing uveoscleral outflow.

availability of topical carbonic anhydrase inhibitors, chronic use is infrequent. Pressure-lowering effect is maximal with full-dose acetazolamide, with slightly less effect from systemic methazolomide and topical dorzolamide.

Topical

●Dorzolamide 2% b.i.d. to t.i.d.

●Brinzolamide 1% b.i.d. to t.i.d.

●Decreases IOP as much as 25% through a decrease in aqueous production.

●Additive to β-blockers (further 10% to 20% decrease in IOP).

Side effects:

●Stinging on instillation, greater with dorzolamide than brinzolamide because of lower pH of dorzolamide;

●Ocular allergy and sensitivity, approximately 20%.

With significantly fewer side effects than the systemic carbonic anhydrase inhibitors, dorzolamide has become a valuable second-line and, sometimes, first-line medication.

Combination β-blockers and carbonic anhydrase inhibitors

●Timolol 0.5% and dorzolamide 2% b.i.d.

The ease of use of a single eyedrop may improve compliance

tion of periocular skin;

●Increases eyelash thickness, number, length and color;

●Anterior uveitis and cystoid macular edema reported; aphakic and pseudophakic eyes with open posterior capsules may be at greater risk with incidence of approximately 5% in these eyes;

●Recurrence of herpes simplex hepatitis has been reported.

better effect than concomitant treatment with two different medications. Ocular and systemic side effects are comparable in incidence to those of timolol and dorzolamide.

Parasympathomimetic agonists

Parasympathomimetic agents decrease IOP by 20% by increasing the facility of outflow.

Direct acting (cholinergic)

●Pilocarpine hydrochloride 0.25%, 0.5%, 1% to 6%, 8%, and 10%, (multiple brands, including generic) b.i.d. to q.i.d.

●Pilocarpine nitrate 1%, 2%, and 4% b.i.d. to q.i.d.

●Pilocarpine hydrochloride gel 4% QHS.

●Pilocarpine slow release (20 equivalent to 2% pilocarpine, 40 equivalent to 4% pilocarpine) every 5 to 7 days.

Laser therapy: selective laser trabeculoplasty

Similar to ALT, but avoids thermal response in trabecular meshwork cells, instead inducing a primarily biologic response. Retreatment believed to be more successful in SLT than ALT.

Surgical

Filtration surgery

peutic effects.

Direct and indirect acting

●Carbachol 0.75%, 1.5%, 2.25%, and 3% qd to t.i.d.

Indirect acting

●Echothiophate iodide 0.03%, 0.06%, 0.125%, and 0.25% qd to b.i.d.

●Demecarium bromide 0.125% and 0.25% qd to b.i.d.

Side effects:

●Cholinergic: nausea, vomiting and diarrhea, and pulmonary congestion due to increased pulmonary secretion;

●Ocular: ciliary muscle contraction resulting in pain and fluctuating myopia, miosis resulting in decreased vision, especially at nighttime; increased incidence of cataracts, detached retina, especially with stronger, indirect-acting sympathomimetic agents;

into the eye near the limbus is made beneath the conjunctiva and a partial-thickness scleral flap. The scleral flap offers some resistance to the egress of aqueous, minimizing the chances of hypotony, and the resultant conjunctival bleb allows diffusion of the aqueous through the conjunctiva onto the surface of the eye.

In eyes without previous surgery, the success rate is approximately 75%. In eyes with previous surgery, the success rate is lower. In blacks and in younger patients, the success rate is believed to be lower as well because of more rapid healing and scarring.

Traditionally, filtration surgery has been performed only after medical and laser therapy have failed. Recent studies suggest that initial surgery may be equally beneficial and as cost effective as medical or laser therapy.

Surgical complications

Hemorrhage, infections, and wound leaks, although rare, are

tylcholine esterase. Because of systemic absorption, the body is depleted of acetylcholine esterase and pseudocholine esterase with chronic use; if the muscle relaxant succinylcholine is used in general anesthesia, prolonged respiratory paralysis may occur.

Parasympathomimetic agents are additive to β-blockers and carbonic anhydrase inhibitors, and partially additive to latanoprost.

Because of ocular side effects, they are relegated to a secondor third-line medication.

Laser therapy: argon laser trabeculoplasty

●Successful in decreasing IOP in 90% of adult OAG.

●Average decrease 4 to 8 mmHg.

●In general, the higher the IOP, the greater the absolute and percentage decrease in IOP

●Approximately 55% still under control after 5 years.

●Retreatment possible but success rate lower, duration of effect not as long, and post-treatment elevation of IOP more frequent.

●More effective in older patients than in younger patients.

Complications

●Post-treatment iritis, inflammation, and transient elevation of IOP common.

●Few serious complications.

Indications

●Usually tried after medical therapy is ineffective or intolerable.

●Initial treatment with argon laser possibly beneficial for some patients.

Contraindications

●Glaucoma secondary to iritis, angle recession, neovascularization of the angle, or congenital glaucoma.

the eye undergoing a filtration operation include hypotony, flat anterior chamber, choroidal effusion, and suprachoroidal hemorrhages in the perioperative period, with progression of cataract, failure of filtration, and endophthalmitis occurring as late problems.

The postoperative use of 5-fluorouracil and the intraoperative use of mitomycin C to decrease fibrosis and scarring increase the chances of successful filtration and have found wide acceptance, especially for high-risk eyes. This gain in greater filtration is offset by an increased incidence of persistent wound leak, hypotony maculopathy, and late-onset endophthalmitis.

Because the incidence of endophthalmitis in a filtered eye is at least 1% per year, proper education of the patient regarding early infection (‘blebitis’) is critical in preventing this blinding complication. Early treatment of blebitis with topical antibiotics and steroids is almost always effective.

Tube-shunt procedures

When excess conjunctival scarring from previous surgery limits the chances for successful trabeculectomy, various tube-shunt implants may be placed to drain aqueous from the anterior chamber to a mechanically maintained subconjunctival space posterior to the limbus.

All of the different implants share the common problems of blockage of the internal or external ostia of the drainage tube, external erosion of the implant, hypotony, insufficient IOP lowering, and fibrosis of the conjunctival space.

Generally, these procedures are reserved for eyes in which standard surgery has failed.

Cyclodestructive procedures

When all attempts at filtration surgery, with or without an implant, have failed and the IOP is still too high, a cyclodestructive procedure may be considered. By destroying the ciliary processes, the source of aqueous production, the IOP is lowered.

of lens protein only rarely causes an immune response has led investigators to conclude that an alteration in the natural tolerance of the body to lens protein is essential for lens protein to become antigenic; this process seems to be T-cell mediated.

Phacoanaphylactic endophthalmitis may occur after penetrating ocular trauma involving the lens, ‘uncomplicated’ extracapsular cataract surgery, or cataract extraction complicated by posterior luxation of lens material.

COURSE

Onset of inflammation may be as early as 24 hours after a lens injury (although this is more consistent with an infectious cause) or as late as 2 weeks after a lenticular insult. The condition typically presents 3 to 5 days after injury in patients already sensitized to lens protein, whereas 10 to 14 days is more common after initial lens injury.

DIAGNOSIS

Clinical signs and symptoms

Clinically, phacoanaphylactic endophthalmitis may present with a spectrum of signs ranging from a mild anterior uveitis to a severe hypopyon uveitis resembling infectious endophthalmitis.

Ocular

●Eyelid edema.

●Anterior chamber cells and flare.

●Hypopyon.

●Corneal edema.

●Mutton-fat precipitates.

●Striae in Descemet’s membrane.

●Conjunctival chemosis, hyperemia.

●Anterior and/or posterior synechiae.

●Pupillary membranes.

●Pupillary seclusion.

●Decreased vision.

●Retinal detachment.

●Secondary glaucoma.

diagnosis is imperative to preserve visual function because prolongation of either leads to irreversible damage to ocular structures.

TREATMENT

Aggressive treatment, directed at the most likely cause, is essential; prompt suppression of inflammation to prevent the destruction of ocular tissues by the inflammatory process is the hallmark of therapy. Whenever possible, this may be facilitated by:

●Vitrectomy to remove retained lens material.

Ocular

Vigorous anti-inflammatory therapy consistent with the severity of inflammation should be initiated without delay. Highdose systemic corticosteroids such as:

●Prednisone 80 to 120 mg/day may bring rapid improvement; the dose should be tapered as rapidly as possible.

The therapeutic armamentarium also includes topical corticosteroids:

●Prednisolone acetate 1.0% every hour; and/or

●Sub-Tenon’s injections* of corticosteroids (preferably aqueous, not depot).

Cycloplegic/mydriatic agents also can be beneficial.

As the inflammation subsides, the gradual dissolution of intravitreal retained lens material can be monitored with ultrasonography.

REFERENCES

Hodes BL, Stern G: Phacoanaphylactic endophthalmitis: echographic diagnosis of phacoanaphylactic endophthalmitis. Ophthalm Surg 7:60–64, 1976.

Marak G: Phacoanaphylactic endophthalmitis. Surv Ophthalmol 36:325– 339, 1992.

Smith RE, Weiner P: Unusual presentation of phacoanaphylactic endophthalmitis following phacoemulsification. Ophthalm Surg 7:65–68, 1976.

DIAGNOSIS

Because endophthalmitis can have a toxic, mechanical, or infectious cause, a careful history (particularly with respect to recent ocular trauma and concomitant systemic infections) is vital.

Diagnostic ultrasonography is helpful to compensate for hazy media, in identifying retained intravitreal lens material, and to visualize early vitreous organization, indicating the need for prompt vitrectomy and possible intravitreal corticosteroids.

Diagnostic vitrectomy may be performed in an attempt to isolate infectious organisms, depending on the severity of the inflammation. Although intensive systemic and intravitreal antibiotics are essential to salvage an infected eye, they are of no value in the management of phacoanaphylactic endophthalmitis.

Differential diagnosis

Phacoanaphylactic endophthalmitis is readily confused with infectious endophthalmitis; in both conditions, early etiologic

274 PIGMENTARY DISPERSION SYNDROME AND PIGMENTARY GLAUCOMA 365.13

James A. Savage, MD

Henderson, Nevada

ETIOLOGY/INCIDENCE

Pigmentary glaucoma is a chronic open-angle glaucoma characterized by loss of pigment from the iris pigment epithelium and its subsequent deposition onto structures of the anterior and posterior chambers. Such pigment shedding and deposition are normal consequences of aging, but occasionally are so pronounced that they constitute pigmentary dispersion syndrome

(PDS). In PDS, the shedding of pigment is evident as midperipheral radial iris transillumination defects (Figure 274.1). The

metry may be due to concurrent unilateral development of exfoliative syndrome (increases pigment deposition in affected eye), cataract formation with increased relative pupillary block (decreases), or miosis (e.g. with Horner’s syndrome [decreases]).

If pigment dispersion is unilateral, it is important to rule out ocular neoplasm, especially ocular melanoma.

Pigmentary glaucoma

All of the findings for PDS exist plus decreased outflow facility, elevated intraocular pressure, and typical glaucomatous optic nerve and visual field damage.

concavity of the midperipheral iris, iridozonular contact, and, hence, the shedding of pigment. Pilocarpine and other parasympathomimetics have the disadvantage of frequent side effects of brow ache and blurred vision, especially in young patients. In addition, there is an increased risk of retinal detachment with the use of parasympathomimetics in this typically myopic population. Pilocarpine in the form of Pilopine-HS gel or Ocuserts may offer a more gradual, steady, and better tolerated effect than pilocarpine drops every 6 hours.

Dapiprazole, a selective a-adrenergic blocker, produces miosis without cyclotonia and therefore may be much better tolerated than parasympathomimetics such as pilocarpine.

Differential diagnosis

●Normal eyes with aging (trabecular pigment less marked and less circumferential than in PDS).

●Exfoliative syndrome (older patients, more often unilateral, exfoliative material visible, iris transillumination defects at pupillary margin rather than in its midperiphery).

●Secondary pigmentary glaucoma after cataract extraction and posterior chamber intraocular lens implantation (more common if lens in sulcus than in capsular bag, iris transillumination defects correspond to the location of intraocular lens haptics and/or optic).

●Uveitis (iris transillumination defects such as with herpes zoster or other anterior uveitis, pigment dispersion with anterior uveitis, and pigment granules in anterior chamber from PDS, which may be confused with inflammatory cells).

●Ocular neoplasms (usually unilateral):

●Iris ring melanoma;

●Other ocular melanoma;

●Cysts and other neoplasms of iris and ciliary body.

●Melanocytosis (usually unilateral).

●Ocular trauma:

●Surgical and accidental;

●Hyphema;

●Angle recession;

●Ghost cell glaucoma (confusion between khaki-colored erythroclasts and liberated pigment granules).

●Acute angle closure.

●Amyloidosis.

●Ocular irradiation.

●Siderosis.

●Hemosiderosis.

●Rhegmatogenous retinal detachment.

●Diabetes mellitus.

●Adie’s pupil.

TREATMENT

Treatment is similar to that for primary open-angle glaucoma. Patients with PDS should be followed as glaucoma ‘suspects,’ with periodic evaluation of intraocular pressure, optic nerve, and visual fields. Also, the clinician should document changes

Surgical

Laser therapy

●Argon and selective laser trabeculoplasty:

●Appear to have equivalent efficacy;

●Longer-term success is better in younger patients (suggests an increased resistance to the beneficial effects of laser as the disease progresses over time);

●There may be dramatic improvement in intraocular pressure, but there is some risk of a transient or lasting increase in intraocular pressure after trabeculoplasty;

●Titrate the laser power to the minimum required to generate the desired visible effect on the trabecular meshwork.

●Laser iridectomy:

●The contour of the midperipheral iris is changed (possibly eliminates ‘reverse pupillary block’);

●Its beneficial effect might be to interrupt the process of pigment shedding/deposition/trabecular damage rather than to immediately lower the intraocular pressure.

●Argon laser iridoplasty:

●Efforts to flatten the iris and to decrease iridozonular contact with this technique have not shown promise. In addition, inflammation and liberation of pigment from this technique may cause temporary or lasting worsening of intraocular pressure, and the iris concavity can actually be worsened. In view of these findings, the technique appears to be contraindicated in PDS and pigmentary glaucoma.

Filtration surgery

●The success of glaucoma filtration surgery for pigmentary glaucoma appears to be similar to that in primary openangle glaucoma.

COMPLICATIONS

The side effects of glaucoma medications in general apply. The side effects of miotics, in particular, are ciliary spasm and retinal detachment in this young and myopic population. Increased intraocular pressure after laser procedures may be transient or lasting. The usual possible complications of filtration surgery also apply.

REFERENCES

Campbell DG: Pigmentary dispersion and glaucoma: A new theory. Arch Ophthalmol 97:1667–1672, 1979.

Farrar SM, Shields MB: Current concepts in pigmentary glaucoma. Surv Ophthalmol 37:233–252, 1993.

Farrar SM, Shields MB, Miller KN, et al: Risk factors for the development and severity of glaucoma in the pigment dispersion syndrome. Am J Ophthalmol 108:223–229, 1989.

Migliazzo CV, Shaffer RN, Nykin R, et al: Long-term analysis of pigmentary dispersion syndrome and pigmentary glaucoma. Ophthalmology 93:1528–1536, 1986.

Sugar HS, Barbour FA: Pigmentary glaucoma: a rare clinical entity. Am J Ophthalmol 32:90–92, 1966.

275 PLATEAU IRIS 743.8

Robert Ritch, MD

New York, New York

Clement Chee Yung Tham MD, FRCS, FCOphth(HK)

Hong Kong, China

The term ‘plateau iris’ was first used by Tornquist in 1958 to describe an anatomic configuration in which the iris is inserted anteriorly on the ciliary body face and the iris root angulates forward and then centrally. The result is somewhat akin to a bird’s-eye view of a mesa (hence the name): the iris surface appears flat and the anterior chamber deep on slit lamp examination, but the angle is narrow on gonioscopy, with a sharp drop-off of the peripheral iris. By contrast, in pupillary block angle-closure glaucoma, the most common form of angleclosure glaucoma, the anterior chamber is shallow and the iris surface tends to be convex (iris bombé) (Figure 275.1).

Despite laser iridotomy, the angle of an eye with plateau iris can remain narrow, and the angle can be closed either spontaneously or by dilating the pupil, thus resulting in angle closure.

This situation is uncommon. Plateau iris syndrome refers to the development of angle closure, either spontaneously or after pupillary dilation, in an eye with plateau iris configuration despite the presence of a patent iridectomy or iridotomy. Some patients may develop elevated intraocular pressure (IOP) or even acute angle-closure glaucoma.

ETIOLOGY/INCIDENCE

Plateau iris results from large and/or anteriorly positioned ciliary processes holding up the peripheral iris and maintaining its apposition to the trabecular meshwork. Two subtypes exist, differentiated according to the level of the structures on the angle-wall occludable by the iris, or the ‘height’ to which the plateau rises. In the complete syndrome, which comprises the classic situation and is rare, the angle closes to the upper trabecular meshwork or Schwalbe’s line, and IOP rises when the angle closes with pupillary dilation. In the incomplete syndrome, which is far more common, the angle closes partially, leaving the upper portion of the filtering meshwork open, and IOP does not change. The incomplete syndrome is clinically significant in that these patients can develop PAS months to years after a successful iridotomy produces what appears as a well-opened angle.

Patients with plateau iris tend to be female, younger (30s to 50s) and less hyperopic than those with relative pupillary block, and often have a family history of angle-closure glaucoma. The fact that iridociliary apposition in plateau iris syndrome persists after cataract extraction suggests that this is a heritable anatomic configuration and not secondary to lens size or position. The younger the patient, the greater the component of angle-crowding by the plateau configuration and the less pupillary block necessary for occludability. Most patients, however, have some element of relative pupillary block superimposed upon a plateau iris configuration, but the extent of pupillary block necessary to induce angle-closure is accordingly less in eyes with plateau iris.

FIGURE 275.1. High frequency ultrasound image of plateau iris syndrome.

COURSE/PROGNOSIS

If plateau iris syndrome is not diagnosed and treated properly, repeated episodes of angle closure can produce peripheral anterior synechiae and permanent elevation of IOP. The angle can narrow progressively with age due to enlargement of the lens, so that an angle with plateau configuration which does not close after iridotomy may do so some years later. Periodic gonioscopy is required. Argon laser peripheral iridoplasty (ALPI) is the definitive treatment for plateau iris. It is highly effective in eliminating residual appositional closure after laser iridotomy caused by plateau iris syndrome and the effect is maintained for years, although a small proportion of patients may require retreatment.

DIAGNOSIS

The diagnosis of plateau iris configuration can be made with indentation gonioscopy prior to iridotomy. A diagnosis of plateau iris syndrome, however, requires prior elimination of any component of pupillary block by iridotomy.

The anterior chamber is usually of medium depth and the iris surface slightly convex. On gonioscopy, the iris root angu-

lates forward and then centrally. In relative pupillary block, indentation gonioscopy pushes the iris root posteriorly, opening the angle. In plateau iris, the ciliary processes prevent posterior movement of the peripheral iris, resulting in a configuration in which the slit beam follows the curvature of the iris to its deepest point at the periphery of the lens where the ciliary processes begin, then rises again over the ciliary processes before dropping peripherally (double hump sign). Greater force is needed to open the angle than in pupillary block because the ciliary processes must be displaced, and the angle does not open as widely.

weak miotic therapy, such as 2% pilocarpine at bedtime, may open the remaining angle.

If plateau iris configuration is diagnosed incidentally in an eye with an open angle, caution should be exercised in dilation and the patient followed gonioscopically at routine intervals for signs of progressive angle closure. If the angle continues to be narrow, it is sometimes difficult to determine if there is progressive closure of the angle. Monitoring the eye with indentation gonioscopy is valuable for showing progressive angle closure.

Differential diagnosis

If the patient presents with elevated IOP, careful indentation gonioscopy should be performed, as in all cases of glaucoma, so that the condition is not confused with open-angle glaucoma because of the normal depth of the anterior chamber and relatively flat iris surface on direct examination. The most common cause of differential diagnostic confusion on routine examination is a prominent peripheral iris roll. With this iris picture, however, the peripheral iris does not occlude the angle on dilation, and it does not predispose to angle-closure glaucoma.

If the angle remains closed after iridotomy for pupillary block, the first step in the differential diagnosis is to determine whether the closure is appositional or synechial by indentation gonioscopy. If appositional, plateau iris can be diagnosed as above. The other two categories of angle-closure in the differential are phacomorphic glaucoma (intumescent lens) and malignant (ciliary block, aqueous misdirection) glaucoma, in which the anterior chamber is flat or extremely shallow.

Iris and ciliary body cysts can also produce acute or chronic angle-closure. These produce a plateau iris type of configuration (pseudo-plateau iris) and are usually easily diagnosed, as the angle is closed either in one quadrant only or, if there are multiple cysts, intermittently. However, when angle closure mimicking pupillary block occurs, a high index of suspicion and careful gonioscopy are needed to distinguish it from ciliary body and iris cysts.

PROPHYLAXIS

If the angle is spontaneously or pharmacologically occludable with closure above the level of the scleral spur, argon laser peripheral iridoplasty is indicated.

TREATMENT

Treatment must be targeted at the cause of angle-closure, in this case the ciliary body and iris root. If pupillary block is either not a component mechanism of the angle-closure or has been eliminated by iridotomy, it is necessary to find a way to eliminate the physical blockage of the angle. Argon laser peripheral iridoplasty compresses the iris root and creates a space where none was before. This procedure alters the configuration of the plateau iris periphery to remove the sharp angulation. Laser settings of 500 microns spot size, with an exposure time of 0.5 second, and an intensity of 200 to 300 mW achieve sustained contraction of the peripheral iris. If miotics are needed for control of IOP after iridotomy, then iridoplasty is indicated only if the angle remains spontaneously appositionally closed on miotics. If iridoplasty does not relieve all the apposition,

REFERENCES

Lowe RF: Plateau iris. Aust J Ophthalmol 9:71, 1981.

Pavlin CJ, Ritch R, Foster FS: Ultrasound biomicroscopy in plateau iris syndrome. Am J Ophthalmol 113:390–395, 1992.

Ritch R: Plateau iris is caused by abnormally positioned ciliary processes. J Glaucoma 1:23–26, 1992.

Ritch R, Tham CCY, Lam DSC: Argon laser peripheral iridoplasty in the management of plateau iris syndrome: long-term follow-up. Ophthalmology 111:104–108, 2004.

Wand M, Pavlin CJ, Foster FS: Plateau iris syndrome: ultrasound biomicroscopic and histological study. Ophthalmic Surg 24:129, 1993.

276PRIMARY ANGLE-CLOSURE GLAUCOMA 365.20

(Primary Closed-Angle Glaucoma)

Emily Patterson, MD

Portland, Oregon

ETIOLOGY/INCIDENCE

Primary angle-closure glaucoma is caused by increased intraocular pressure due to obstruction of aqueous humor outflow from the anterior chamber, which results from closure of the angle by the peripheral root of the iris. It is a bilateral disease and affects patients with anatomically narrow angles. The trabecular meshwork is structurally and functionally normal before closure of the angle takes place.

In its early stages, closure of the angle is nothing more than contact between the trabecular meshwork and the root of the iris, and it is reversible once pupillary block is eliminated. Over time, however, the root of the iris develops adhesions to the trabecular meshwork, forming peripheral anterior synechiae that cannot be relieved by breaking the pupillary block.

Although the mechanism of the pressure rise is the same in each patient, symptoms vary markedly depending on the magnitude and speed of the intraocular pressure rise.

●Angle shallowing, and then closure, develops in eyes with an anatomically narrow anterior chamber angle.

●Relative pupillary block, which obstructs the flow of the aqueous from the posterior chamber into the anterior chamber, plays an important role in the pathogenesis of the disease.

●The condition usually occurs in those older than 40, with a predilection for women. This is because as the lens ages, it grows in its anterior-posterior diameter and crowds the anterior chamber. Women are believed more susceptible because their eyes are slightly smaller.

With prodromal or intermittent angle-closure glaucoma, symptoms are caused by the rapid elevations and decreases of the intraocular pressure. A steamy, hazy cornea is caused by the abrupt rise in pressure as a result of sudden angle occlusion. Symptoms classically include foggy or hazy vision with rainbowcolored haloes around lights. Ocular congestion or discomfort may occur. Symptoms spontaneously subside in a few hours if the pupillary block is relieved by miosis. The miosis may occur when the patient goes to a brighter environment or goes to sleep.

In the acute attack of primary angle-closure glaucoma, the symptoms are precipitated by pupillary dilation resulting from mydriatic drops, dim light, or emotional upset. Once angle closure is established, the symptoms of the intermittent or prodromal attack intensify and endure; they include blurred vision and haloes, conjunctival injection, and severe pain. In addition, nausea and vomiting may occur and are due to autonomic stimulation.

In chronic primary angle-closure glaucoma, the intraocular pressure rises insidiously as the closed area of the angle gradually increases, and patients may be totally free from symptoms or may experience some ocular discomfort and haloes. This variant may mimic chronic open-angle glaucoma if the gonioscopic findings are missed.

DIAGNOSIS

Clinical signs and symptoms

Ocular

Two major subtypes of primary angle-closure glaucomaacute angle-closure glaucoma (indicated as A) and chronic angle-closure glaucoma (indicated as C) show different ocular signs:

●Anterior chamber: shallow (A and C), flare (A), clear (C);

●Chamber angle: closed (A and C) or narrow (C);

●Conjunctiva: chemosis (A), hyperemia (A);

●Hyperosmotic agents are preferred to break an acute attack: oral glycerin in a 50% solution at a dose of 2 to 3 ml/kg, oral isosorbide in doses of 1 to 2 g/kg is preferred in patients with diabetes, and isosorbide is usually tolerated better than glycerin.

●In patients with nausea or vomiting, 20% mannitol IV may be given in a dose of 1 to 2 g/kg, although 500 mg of acetazolamide IV is better.

Ocular

●Treatment is indicated to break an acute attack and control the intraocular pressure until laser iridotomy can be performed, or to manage residual glaucoma after an acute incident.

●Cholinergic agents should be used to pull the iris away from the angle in the eyes in acute attack: one or two drops of 1% to 3% pilocarpine every 5 minutes for 4 doses and then every 1 to 2 hours.

●In an acute case, β-adrenergic-blocking agents, topical carbonic anhydrase inhibitors, and prostaglandin analogs may be added to the regimen of miotics. Corticosteroids (e.g. 1% prednisolone acetate), are useful in controlling inflammation. Dipivefrin is contraindicated before iridotomy, and brimonidine may be less effective or ineffective.

●In a chronic case, medical treatment without laser iridotomy should be temporary.

●The treatment of chronic angle-closure glaucoma after laser iridotomy is similar to that of primary open-angle glaucoma.

Surgical

The treatment of primary angle-closure glaucoma consists of laser iridotomy or peripheral surgical iridectomy after the intraocular pressure has been normalized. In acute angle-closure glaucoma, the eye should be operated on promptly. Iridectomy may be done surgically, or argon or Q-switched Nd:YAG laser may be used to create an iridotomy (laser iridotomy). If the

rior synechiae (A and C), posterior synechiae (A), sector atrophy, usually in the upper half (A);

●Lens: glaukomflecken (A);

●Pupil: dilation, vertical ovalization, mid-dilated, fixed position (A);

●Miscellaneous: increased intraocular pressure (A and C), visual field defects (A and C).

Differential diagnosis

●Chronic angle-closure glaucoma can be differentiated from primary open-angle glaucoma with a narrow angle by gonioscopy.

if intraocular pressure is completely normalized with medical therapy, in order to prevent progression to synechial angle closure. Filtration surgery should not be performed unless iridotomy has failed to normalize the intraocular pressure.

Other

●The patient with acute primary angle-closure glaucoma should be hospitalized to initiate the intensive medical therapy that is usually a prelude to surgery.

●Analgesics may be used to control pain; the administration of 300 to 600 mg of aspirin every 6 to 8 hours is usually adequate.

COMPLICATIONS

Intravenous hyperosmotic agents cause headache, dizziness, nausea, and vomiting; oral glycerin particularly tends to induce nausea. Urinary retention may be brought about by intense diuresis. Pulmonary edema and congestive heart failure may be precipitated in elderly patients with borderline cardiac and renal function; this is especially true of mannitol, which greatly increases blood volume. Cellular dehydration, including cerebral dehydration, occurs more often with mannitol and may result in mental disorientation.

of its safety and convenience. Occasionally an iridotomy may fibrose and close, especially in the setting of intraocular inflammation, and may need to be repeated once or more before it remains open.

Chronic primary angle-closure glaucoma should also be treated surgically even when the intraocular pressure is normalized with medication. Because pupillary block cannot be eliminated by medical therapy, peripheral anterior synechiae will progress in the setting of chronic or intermittent angle closure, regardless of the intraocular pressure.

COMMENTS

Acute primary angle-closure glaucoma is an ophthalmic emergency and requires immediate medical therapy. All medical measures should be used simultaneously to normalize the elevated intraocular pressure. Once the pressure is brought under control, indentation gonioscopy with a Zeiss four-mirrored lens or other indirect goniolens is necessary to confirm the diagnosis and to evaluate the extent of peripheral anterior synechiae. The more extensive the peripheral anterior synechiae, the more likely that antiglaucoma medications will be needed to maintain a normal intraocular pressure after iridotomy. The fellow eye should also be treated with topical miotics to avoid an acute attack until iridotomy can be performed on it as well. Prophylactic laser iridotomy is preferable to surgical iridectomy because

REFERENCES

Fleck BW, Fairley EA: A randomized prospective comparison of operative peripheral iridectomy and Nd:YAG laser iridotomy treatment of acute angle closure glaucoma: 3 year visual acuity and intraocular pressure control study. Br J Ophthalmol 81:884–888, 1997.

Sakuma T, Sawada A, Yamamoto T, et al: Appositional angle closure in eyes with narrow angles: An ultrasound biomicroscopic study. J Glaucoma 6:165–169, 1997.

Saw SM, Gazzard G, Friedman DS: Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology 110(10):1867–1868, 2003.

Sugar HS: Surgical decision, technique and complications of peripheral iridectomy for angle-closure glaucoma. Ann Ophthalmol 7:1237–1241, 1975.

Wolfs RCW, Grobbee DE, Hofman A, et al: Risk of acute angle-closure glaucoma after diagnostic mydriasis in nonselected subjects: The Rotterdam study. Invest Ophthalmol Vis Sci 38:2683–2687, 1997.