- •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
blockers are more likely to be beneficial. (See Chapter 8.)
Bhandari A, Crabb DP, Poinoosawmy D, Fitzke FW, Hitchings RA, Noureddin BN. Effect of surgery on visual field progression in normal-tension glaucoma. Ophthalmology. 1997;104(7):1131–1137.
Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Am J Ophthalmol. 1998;126(4):487– 497.
Collaborative Normal-Tension Glaucoma Study Group. The effectiveness of intraocular pressure reduction in the treatment of normal-tension glaucoma. Am J Ophthalmol. 1998;126(4):498–505.
Mikelberg FS. Normal tension glaucoma. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2000, module 12.
The Glaucoma Suspect
A glaucoma suspect is defined as an individual who has an optic nerve or nerve fiber layer defect suggestive of glaucoma (enlarged cup–disc ratio, asymmetric cup–disc ratio, notching or narrowing of the neuroretinal rim, a disc hemorrhage, or suspicious alteration in the nerve fiber layer) in the absence of an abnormality in visual function as determined by perimetry; or who has a visual field abnormality consistent with glaucoma in the absence of a corresponding glaucomatous optic disc abnormality. Patients with such findings are typically monitored for the development of glaucoma with periodic evaluation of the optic nerve, retinal nerve fiber layer, and visual field. The increasing use of short-wavelength automated perimetry (SWAP) and frequency-doubling technology (FDT) perimetry, as well as assessment of the pattern electroretinogram, may improve the ophthalmologist’s ability to recognize early glaucomatous visual function loss in patients considered to be glaucoma suspects because of a suspicious optic disc appearance (see Chapter 3). If signs of optic nerve damage are present, the diagnosis of early POAG should be considered and treatment initiated. However, in uncertain cases, the ophthalmologist should not hesitate to closely monitor patients without therapy to confirm either initial findings or progressive change, with the aim of better establishing the diagnosis prior to initiating therapy. It may be difficult to classify a glaucoma suspect who has elevated IOP and structural or functional findings that are suggestive but not firmly diagnostic of glaucomatous optic neuropathy. Such patients do not fit neatly into one diagnostic category.
Ocular Hypertension
Some authors consider patients with OHT to be glaucoma suspects. In this book, we define OHT as a condition in which the IOP is elevated above an arbitrary cutoff value, typically 21 mm Hg, in the absence of optic disc, retinal nerve fiber layer, or visual field abnormalities. Estimates of the prevalence of OHT vary considerably; some authorities believe the prevalence of OHT may be as high as 8 times that of definite POAG. Analysis of studies that have observed individuals with elevated IOP for variable periods indicates that the higher the baseline IOP, the greater the risk of developing glaucoma. However, it is important to note that even among individuals with elevated IOP, the majority never develop glaucoma.
Differentiating between diagnoses of OHT and early POAG is often difficult. The ophthalmologist must look carefully for signs of early damage to the optic nerve, such as focal notching, asymmetry of cupping, optic disc hemorrhage, nerve fiber layer defects, or subtle visual field defects.
There is no clear consensus about whether elevated IOP should be treated in the absence of signs of early damage. Some clinicians, after assessing all risk factors, select and treat those individuals
thought to be at greatest risk of developing glaucoma. In OHTS, patients 40–80 years of age with IOP between 24 and 32 mm Hg were randomized to observation or to the reduction of IOP by topical medications (Fig 4-1; see Clinical Trial 4-2 at the end of this chapter). In this study, 4.4% of patients treated (with topical glaucoma medications to reduce IOP 20%) progressed to glaucoma during a 5- year period, based on the development of optic nerve or visual field damage. More than twice as many of the untreated observation group, or 9.5%, progressed. Thus, topical medications were definitively shown to reduce the risk of progression to glaucoma in patients with OHT; however, most untreated patients did not get worse over a 5-year period. Each millimeter of mercury of elevated baseline IOP increased the risk of glaucomatous change by 10%. For each 0.1 increment in vertical cup–disc ratio, the risk was increased by 32%.
Figure 4-1 The number and percentage of participants in the Ocular Hypertension Treatment Study observation group that developed primary open-angle glaucoma (POAG) as a function of baseline intraocular pressure (IOP) and central corneal
thickness (CCT). (Reprinted with permission from Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:718, Fig 1. Copyrighted 2002, American Medical Association.)
OHTS identified older age, higher IOP, lower CCT, higher pattern standard deviation on standard automated perimetry, and higher cup–disc ratio at baseline as important risk factors for the development of POAG. Data from OHTS and the European Glaucoma Prevention Study were combined to create a risk calculation model to predict the 5-year risk of conversion from OHT to glaucoma based on these risk factors.
It has been recognized that variations in CCT affect the IOP measurement. For example, a thicker cornea resists indentation by applanation, resulting in a higher IOP reading. But the increased risk of progression attributed to lower CCT in OHTS was not fully explained by the estimated artifactual error in measured IOP. It is therefore hypothesized that lower CCT may be a marker for other susceptibility factors. Other potential risk factors, such as myopia, diabetes mellitus, positive family
