- •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
Table 1-2
Combined-Mechanism Glaucoma
Most commonly, combined-mechanism glaucoma occurs in a patient who has been successfully treated for a narrow angle but who continues to demonstrate reduced outflow facility and elevated IOP in the absence of peripheral anterior synechiae (PAS). However, combined-mechanism glaucoma can appear in a patient who has open-angle glaucoma but develops secondary angle closure from other causes. In this condition, IOP elevation can occur as a result of the following:
the intrinsic resistance of the trabecular meshwork to aqueous outflow in open-angle glaucoma the direct anatomical obstruction of the filtering meshwork by synechiae in angle-closure glaucoma
Epidemiologic Aspects of Glaucoma
Primary Open-Angle Glaucoma
Magnitude of the problem
Primary open-angle glaucoma (POAG) poses a significant public health problem. The estimated prevalence of POAG in the United States in individuals older than 40 years is 1.86% (95% confidence interval, 1.75%–1.96%), based on a meta-analysis of population-based studies. Applied to data from the 2000 US census, this percentage translates to nearly 2.22 million Americans affected. Estimates based on the available data indicate that between 84,000 and 116,000 of them have become bilaterally blind (best-corrected visual acuity ≤20/200 or visual field <20°). With the rapidly aging US population, the number of POAG patients is estimated to increase by 50%, to 3.36 million in 2020.
The World Health Organization (WHO) undertook an analysis of the literature to estimate the prevalence, incidence, and severity of the different types of glaucoma on a worldwide basis. Using data collected predominantly in the late 1980s and early 1990s, the WHO estimated the global population of persons with high IOP (>21 mm Hg) to be 104.5 million. The incidence of POAG was estimated at 2.4 million persons per year. Blindness prevalence for all types of glaucoma was estimated at more than 8 million persons, with 4 million cases caused by POAG. Glaucoma was theoretically calculated to be responsible for 12.3% of blindness. This makes glaucoma the second leading cause of blindness worldwide, following cataract.
Prevalence
The estimated prevalence (the total number of individuals with a disease at a specific time) varies widely across population-based samples, with the Rotterdam Study (northern European population) showing a prevalence of 0.8% and the Barbados Eye Study (Caribbean population) showing a prevalence of 7% in individuals older than 40 years. But in both of these studies, there is a significant increase in the prevalence of glaucoma in older individuals, with estimates for persons in their 70s being generally 3 to 8 times higher than those for persons in their 40s. In addition, multiple population-based surveys have demonstrated a higher prevalence of glaucoma in specific ethnic groups. Among whites aged 40 years and older, a prevalence of between 1.1% and 2.1% has been reported based on population-based studies performed throughout the world. The prevalence among black persons and Latino persons is up to 4 times higher compared to the prevalence among whites. Black individuals are also at greater risk of blindness from POAG, and this risk increases with age: in persons aged 46–65 years, the likelihood of blindness from POAG is 15 times higher among blacks than that among whites.
Friedman DS, Wolfs RC, O’Colmain BJ, et al. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004;122(4):532–538.
Javitt JC, McBean AM, Nicholson GA, Babish JD, Warren JL, Krakauer H. Undertreatment of glaucoma among black Americans. N Engl J Med. 1991;325:1418–1422.
Varma R, Ying Lai M, Francis BA, et al. Prevalence of open-angle glaucoma and ocular hypertension in Latinos: the Los Angeles Latino Eye Study. Ophthalmology. 2004;111(8):1439–1448.
Incidence
The incidence (the number of new cases of a disease that develop during a specific period) of POAG, which has been examined less than the prevalence of POAG in population-based studies, varies widely. The Barbados Eye Study demonstrated, in a predominantly black population, an overall incidence of 2.2% in subjects older than 40 years. A much lower incidence was demonstrated in the Visual Impairment Project, based in Melbourne, Australia (1.1% for definite and probable POAG); and in the Rotterdam Study (5-year risk of 1.8% for definite and probable POAG).
Risk factors
Strictly defined, a factor can be considered a risk factor only if it predates disease occurrence. In prospective studies, a number of risk factors have been found to be associated with progression of glaucoma, including elevated IOP, reduced perfusion pressure, advanced age, thin central corneas, racial background, and a positive family history (Table 1-3). The role of gender and of various systemic factors, such as diabetes, systemic hypertension, and atherosclerotic and ischemic vascular diseases, in the development of glaucoma has been widely debated, and currently available data are inconclusive.
Table 1-3
In terms of the assessment of risk factors, the importance of diurnal variation in IOP has been increasingly recognized. Current evidence, obtained under sleep laboratory conditions, suggests that in most subjects, the peak IOP occurs at night and is therefore not seen in the routine clinical setting.
Dueker DK, Singh K, Lin SC, et al. Corneal thickness measurement in the management of primary open-angle glaucoma: a report by the American Academy of Ophthalmology. Ophthalmology. 2007;114(9):1779–1787.
Hennis AJ, Wu SY, Nemesure B, et al. Nine-year incidence of visual impairment in the Barbados Eye Studies. Ophthalmology. 2009;116(8):1461–1468. Epub 2009 Jun 4.
Leske MC, Heijl A, Hyman L, et al. Predictors of long-term progression in the Early Manifest Glaucoma Trial. Ophthalmology. 2007;114(11):1965–1972.
Primary Angle-Closure Glaucoma
Race
The prevalence of primary angle-closure glaucoma (PACG) varies among different racial and ethnic groups. Among white populations in the United States and Europe, it is estimated at 0.1%. Inuit populations from the Arctic regions have the highest-known prevalence of PACG—20 to 40 times higher than that for whites. Although estimates of the prevalence of PACG in Asian populations vary widely, available data suggest that for most Asian population groups, the prevalence of PACG is between that for whites and that for the Inuit. Some studies have suggested that the prevalence of PACG among blacks is similar to that among whites, with most cases among black persons being of the chronic variety.
Gender
Acute angle-closure glaucoma has been reported more often in women than in men, and several population-based surveys show that women are at increased risk of angle-closure glaucoma. Studies of normal eyes have shown that women have shallower anterior chambers than men.
