- •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
Figure 3-24 High false-positive rate. The top visual field contains characteristic “white scotomata,” which represent areas of impossibly high retinal sensitivity. Upon return visit 3 weeks later, the patient was carefully instructed to respond only when she saw the light, resulting in the bottom visual field, which shows good reliability and demonstrates the patient’s dense superior visual field loss (Humphrey 30-2 program).
Interpretation of a Series of Visual Fields
Interpretation of serial visual fields should meet 2 goals:
1.separating real change from ordinary variation
2.using the information from the visual field testing to determine the likelihood that a change is related to glaucomatous progression
Several methods can be used to analyze a series of visual fields for glaucomatous change. Point-by- point analysis performed with statistical programs available from the major instrument manufacturers (eg, the Humphrey Glaucoma Progression Analysis or Octopus Delta programs) is a valuable aid in progression analysis. Application of these programs is described clearly in the owner’s manual accompanying the program packages. The point-by-point approach is better at identifying regions of change within a visual field.
Another method used in visual field series analysis is comparison of visual field indices, which can reveal global trends that may be missed with point-by-point analysis. Raw perimetric data can also be transferred to independent software programs for change analysis. Even when computed statistical methods are employed, however, separating true pathologic progression from normal test- to-test variability remains a difficult challenge. Moreover, the clinician interpreting a series of visual fields must keep in mind that test variability is increased as part of the pathophysiology of glaucoma.
Whatever method the clinician uses, the fundamental requirement for adequate interpretation over time is a good baseline visual field. Often the patient experiences a learning effect, and the second visual field may show substantial improvement over the first (Fig 3-25). At least 2 visual fields should be obtained as early as possible in the course of a patient’s disease. If they are quite different, a third test should be performed. Subsequent visual fields should be compared with these baseline fields. If a follow-up visual field appears to differ from baseline, the test should be repeated for confirmation.
Figure 3-25 Learning effect. These 3 visual fields were obtained within the first 3½ months of diagnosis in a patient with very early, clinically stable glaucoma. They illustrate the learning effect between the first and the second visual fields. The third visual field is similar to the second, and the second and third visual fields provided a baseline for follow-up of the patient (Humphrey 30-2 program).
Progression
No hard-and-fast rules define what determines visual field progression. But, generally, the methods used in the assessment of progression employ regional or global analysis and an event-based or trend-based approach.
Progressive cases such as that shown in Figure 3-26 are easy to recognize. A general decrease in sensitivity may be secondary to glaucoma or may be related to media opacity, and clinical correlation is required, which is often difficult. Two causes of general decline in sensitivity that may confuse interpretation are variable miosis (often related to use of eyedrops) and cataract (Fig 3-27).
Figure 3-26 Progression of glaucomatous damage. The 3 visual fields shown illustrate the development and advancement of a visual field defect. Between the first and second visual fields, the patient developed a significant inferior nasal step (see the section Patterns of Glaucomatous Nerve Loss). The third visual field illustrates the extension of this defect to the blind spot, as well as the development of superior visual field loss (Humphrey 30-2 program).
Figure 3-27 Pupil size (marked on each visual field). The first visual field shown was obtained before the patient began pilocarpine therapy. The second visual field was obtained with a miotic pupil (Humphrey 30-2 program).
Suspected new defects or progression of existing defects should be reproduced on subsequent visual fields to determine their validity. Definitions of progression have varied in clinical trials; these definitions will continue to be refined in the years to come with further improvements in computer software.
The Glaucoma Change Probability (Fig 3-28) uses an event-based analysis, which is based on the analysis performed in the Early Manifest Glaucoma Trial, to provide a sensitive assessment of possible progression. It compares the current visual field with a baseline composed of 2 separate visual field tests. The operator must choose the 2 baseline visual fields. Thus, with this method, if progression occurs, a new baseline must be established for future analysis.
