- •Contents
- •General Introduction
- •Objectives
- •1 Introduction to Glaucoma: Terminology, Epidemiology, and Heredity
- •Definitions
- •Classification
- •Open-Angle, Angle-Closure, Primary, and Secondary Glaucomas
- •Combined-Mechanism Glaucoma
- •Epidemiologic Aspects of Glaucoma
- •Primary Open-Angle Glaucoma
- •Primary Angle-Closure Glaucoma
- •Genetics, Environmental Factors, and Glaucoma
- •Environmental Factors
- •Genetic Testing
- •Aqueous Humor Formation
- •Suppression of Aqueous Formation
- •Rate of Aqueous Formation
- •Aqueous Humor Outflow
- •Trabecular Outflow
- •Uveoscleral Outflow
- •Tonography
- •Episcleral Venous Pressure
- •Intraocular Pressure
- •Distribution in the Population and Relation to Glaucoma
- •Factors Influencing Intraocular Pressure
- •Diurnal Variation
- •Clinical Measurement of Intraocular Pressure
- •Infection Control in Clinical Tonometry
- •3 Clinical Evaluation
- •History and General Examination
- •Refraction
- •External Adnexae
- •Pupils
- •Biomicroscopy
- •Gonioscopy
- •Direct and Indirect Gonioscopy
- •Gonioscopic Assessment and Documentation
- •The Optic Nerve
- •Anatomy and Pathology
- •Glaucomatous Optic Neuropathy
- •Examination of the Optic Nerve Head
- •The Visual Field
- •Clinical Perimetry
- •Variables in Perimetry
- •Automated Static Perimetry
- •Interpretation of a Single Visual Field
- •Interpretation of a Series of Visual Fields
- •Patterns of Glaucomatous Nerve Loss
- •Manual Perimetry
- •Other Tests
- •4 Open-Angle Glaucoma
- •Primary Open-Angle Glaucoma
- •Clinical Features
- •Risk Factors for POAG Other Than IOP
- •Associated Disorders
- •Prognosis
- •Clinical Features
- •Differential Diagnosis
- •Diagnostic Evaluation
- •Prognosis and Therapy
- •The Glaucoma Suspect
- •Ocular Hypertension
- •Secondary Open-Angle Glaucoma
- •Exfoliation Syndrome
- •Pigmentary Glaucoma
- •Lens-Induced Glaucoma
- •Intraocular Tumors
- •Ocular Inflammation and Secondary Glaucoma
- •Elevated Episcleral Venous Pressure
- •Accidental and Surgical Trauma
- •Schwartz Syndrome (Schwartz-Matsuo Syndrome)
- •Drugs and Glaucoma
- •5 Angle-Closure Glaucoma
- •Introduction
- •Pathogenesis and Pathophysiology of Angle Closure
- •Pupillary Block
- •Angle Closure Without Pupillary Block
- •Lens-Induced Angle-Closure Glaucoma
- •Iris-Induced Angle Closure
- •Primary Angle Closure
- •Risk Factors for Developing Primary Angle Closure
- •Acute Primary Angle Closure
- •Subacute or Intermittent Angle Closure
- •Chronic Angle Closure
- •The Occludable, or Narrow, Anterior Chamber Angle
- •Plateau Iris
- •Secondary Angle Closure With Pupillary Block
- •Lens-Induced Angle Closure
- •Secondary Angle Closure Without Pupillary Block
- •Neovascular Glaucoma
- •Iridocorneal Endothelial Syndrome
- •Tumors
- •Inflammation
- •Aqueous Misdirection
- •Nonrhegmatogenous Retinal Detachment and Uveal Effusions
- •Epithelial and Fibrous Ingrowth
- •Trauma
- •Retinal Surgery and Retinal Vascular Disease
- •Nanophthalmos
- •Persistent Fetal Vasculature
- •Flat Anterior Chamber
- •Drug-Induced Secondary Angle-Closure Glaucoma
- •6 Childhood Glaucoma
- •Classification
- •Genetics
- •Primary Congenital Glaucoma
- •Juvenile Open-Angle Glaucoma
- •Developmental Glaucomas of Childhood With Associated Ocular or Systemic Anomalies
- •Axenfeld-Rieger Syndrome
- •Peters Anomaly
- •Aniridia
- •Sturge-Weber Syndrome
- •Neurofibromatosis
- •Secondary Glaucomas
- •Aphakic Glaucoma
- •Evaluating the Pediatric Glaucoma Patient
- •History
- •Visual Acuity
- •External Examination
- •Anterior Segment Examination
- •Tonometry
- •Central Corneal Thickness
- •Gonioscopy
- •Optic Nerve and Fundus Evaluation
- •Axial Length
- •Other Testing
- •Treatment Overview
- •Surgical Management
- •Medical Management
- •Prognosis and Follow-Up
- •7 Medical Management of Glaucoma
- •Medical Agents
- •Prostaglandin Analogues
- •β-Adrenergic Antagonists
- •Adrenergic Agonists
- •Carbonic Anhydrase Inhibitors
- •Parasympathomimetic Agents
- •Combined Medications
- •Hyperosmotic Agents
- •General Approach to Medical Treatment
- •Open-Angle Glaucoma
- •Angle-Closure Glaucoma
- •Administration of Ocular Medications
- •Use of Glaucoma Medications During Pregnancy or by Nursing Mothers
- •Use of Glaucoma Medications in Elderly Patients
- •Generic Medications
- •Compliance
- •8 Surgical Therapy for Glaucoma
- •Surgery for Open-Angle Glaucoma
- •Laser Trabeculoplasty
- •Incisional Surgery for Open-Angle Glaucomas
- •Combined Cataract and Filtering Surgery
- •Surgery for Angle-Closure Glaucoma
- •Laser Iridotomy
- •Laser Gonioplasty, or Peripheral Iridoplasty
- •Incisional Surgery for Angle Closure
- •Other Procedures to Lower IOP
- •Glaucoma Drainage Device Implantation
- •Ciliary Body Ablation Procedures
- •Nonpenetrating Glaucoma Surgery
- •Special Considerations in the Surgical Management of Elderly Patients
- •Basic Texts
- •Related Academy Materials
- •Requesting Continuing Medical Education Credit
attack, it is important to reevaluate the angle by gonioscopy to assess the degree of residual synechial angle closure and to confirm the reopening of at least part of the angle.
Improved IOP does not necessarily mean that the angle has opened. Because of ciliary body ischemia and reduced aqueous production, the IOP may remain low for weeks following acute angle closure. Thus, IOP may be a poor indicator of angle function or anatomy. A second gonioscopy or serial gonioscopy is therefore essential for follow-up of the patient to be certain that the angle has adequately opened.
Lam DS, Leung DY, Tham CC, et al. Randomized trial of early phacoemulsification versus peripheral iridotomy to prevent intraocular pressure rise after acute primary angle closure. Ophthalmology. 2008;115(7):1134–1140.
Seah SK, Foster PJ, Chew PT, et al. Incidence of acute primary angle-closure glaucoma in Singapore: an island-wide survey. Arch Ophthalmol. 1997;115(11):1436–1440.
Subacute or Intermittent Angle Closure
Subacute or intermittent angle closure is a condition characterized by episodes of blurred vision, halos, and mild pain caused by elevated IOP. These symptoms resolve spontaneously, especially during sleep-induced miosis, and IOP is usually normal between the episodes, which occur periodically over days, months, or years. These episodes are often confused with headaches or migraines. The correct diagnosis can be made only with a high index of suspicion and gonioscopy. The typical history and the gonioscopic appearance of a narrow chamber angle with or without PAS help establish the diagnosis. Such episodes may occur in the absence of symptoms as well, identified by measurement of increased IOP or by identification of PAS in the setting of a narrow angle.
Laser iridotomy is the treatment of choice in subacute angle closure unless significant lens opacity is present, in which case lensectomy is typically curative. This condition can progress to chronic angle closure or to an acute attack that does not resolve spontaneously. With improvements in phacoemulsification, especially in terms of anterior chamber stabilization and fluidic control, primary lensectomy is increasingly recognized as an effective treatment for this disorder. In cases of significant synechial closure, goniosynechialysis may be performed in conjunction with lensectomy to help open the angle and improve trabecular outflow. Such treatment is more definitive than iridotomy but also introduces the additional risks inherent in intraocular surgery.
Chronic Angle Closure
Chronic angle closure may develop after acute angle closure in which synechial closure persists. It may also develop when the chamber angle closes gradually and IOP rises slowly as angle function progressively becomes compromised. The latter form of chronic angle closure, in which there is gradual asymptomatic angle closure, is the most common. Because of the asymptomatic nature of this condition, vision loss may be the presenting complaint. Accordingly, this disease tends to be diagnosed in its later stages and is a major cause of blindness in Asia. Chronic PAC is often referred to as creeping angle closure because of the slow formation of PAS, which advance circumferentially. The cause of the phenomenon is uncertain, but evidence suggests that multiple mechanisms are involved, including pupillary block, abnormalities in iris thickness and position, and plateau iris configuration.
In chronic ACG, permanent PAS are present, as determined by dynamic gonioscopy. The clinical course resembles that of OAG in its lack of symptoms, initial modest elevation of IOP, progressive glaucomatous optic nerve damage, and characteristic visual field loss. Over time, however, IOP can rise precipitously and become more difficult to control. The diagnosis of chronic ACG is frequently overlooked, and it is commonly confused with chronic OAG. Gonioscopic examination of all
glaucoma patients is important for accurate diagnosis.
Even if miotics and other agents lower the IOP, an iridectomy is necessary to relieve the pupillary block component and reduce the potential for further permanent synechial angle closure. Without an iridectomy, the closure of the angle usually progresses and makes the glaucoma more difficult to control. Even with a patent peripheral iridectomy, progressive angle closure can occur, and repeated periodic gonioscopy is imperative. An iridectomy with or without long-term use of ocular hypotensive medication will control the disease in most patients with chronic ACG. Others may require iridoplasty or lensectomy with or without goniosynechialysis. If these measures fail to lower the IOP, subsequent filtering surgery may be necessary.
Alsagoff Z, Aung T, Ang LP, Chew PT. Long-term clinical course of primary angle-closure glaucoma in an Asian population. Ophthalmology. 2000;107(12):2300–2304.
Ritch R, Lowe RF. Angle closure glaucoma: clinical types. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis: Mosby; 1996:821–840.
Ritch R, Lowe RF. Angle closure glaucoma: mechanisms and epidemiology. In: Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis: Mosby; 1996:801–819.
The Occludable, or Narrow, Anterior Chamber Angle
The nomenclature pertaining to the narrow anterior chamber angle may be somewhat misleading. For example, a narrow angle is not synonymous with a diagnosis of glaucoma, but rather an anatomical description. Only a small percentage of patients with shallow anterior chambers develop ACG. Unfortunately, even when performed by experienced clinicians, gonioscopy has relatively poor predictive value for determining which susceptible patients will develop overt angle closure. Many clinicians have attempted to predict which asymptomatic patients with normal IOP will develop angle closure by performing a variety of provocative tests. These tests are designed to precipitate a limited form of angle closure, which can then be detected by gonioscopy and IOP measurement. The methods commonly used include pharmacologic pupillary dilation and the darkroom prone-position test. An IOP increase of 8 mm Hg or more, in conjunction with gonioscopic evidence of appositional angle closure in at least a portion of the angle, is considered a positive result. An asymmetric pressure rise between the 2 eyes with a corresponding degree of angle closure is also considered a positive result. Provocative testing has not been validated in a prospective study; thus, it is rarely used.
The decision to treat an asymptomatic patient with narrow angles rests on the clinical judgment of the ophthalmologist and the accurate assessment of the anterior chamber angle. Any patient with narrow angles, regardless of the results of provocative testing, should be advised of the symptoms of angle closure, of the need for immediate ophthalmic attention if symptoms occur, and of the value of long-term periodic follow-up. An iridotomy is not necessary in all patients with a suspicious or borderline narrow angle. If a patient with a narrow angle has documented appositional or nearappositional closure, PAS, increased segmental trabecular meshwork pigmentation, a history of previous angle closure, a positive provocative test result, or a significant risk of angle closure (ACD of less than 2.0 mm, strong family history), then the ophthalmologist should consider performing an iridotomy. The status of the lens and the benefit of cataract surgery should also be considered in the decision.
Various factors that cause pupillary dilation may induce angle closure. These factors include a variety of drugs, as well as pain, emotional upset, or fright. In predisposed eyes with shallow anterior chambers, either mydriatic or miotic agents can precipitate acute angle closure. Mydriatic agents include not only dilating drops but also systemic medications with sympathomimetic or anticholinergic activity that may cause pupillary dilation. The effect of miotics is to pull the peripheral iris away from the chamber angle. However, strong miotics may also cause the zonular
