- •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 3-28 Glaucoma Change Probability. Progression of glaucomatous damage. Each of the 3 visual fields shown here demonstrates progressive loss compared with the same baseline. The black triangles designate points with a probability (P <
.05) that the value is worse than the baseline value. (Courtesy of Ronald L. Gross, MD.)
Correlation with the optic disc
It is important to correlate changes in the visual field with those of the optic disc. If such correlation is lacking, the ophthalmologist should consider other causes of vision loss, such as ischemic optic neuropathy, demyelinating or other neurologic disease, pituitary tumor, and so forth. This consideration is especially important in the following situations:
The patient’s optic disc seems less cupped than would be expected for the degree of visual field loss.
The pallor of the disc is more impressive than the cupping. The progression of the visual field loss seems excessive.
The pattern of visual field loss is uncharacteristic for glaucoma—for example, it respects the vertical midline.
The location of the cupping or thinning of the neural rim does not correspond to the proper location of the visual field defect.
Anderson DR, Patella VM. Automated Static Perimetry. 2nd ed. St Louis: Mosby; 1999.
Drake MV. A primer on automated perimetry. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 1993, module 8.
Drance SM, Anderson DR, eds. Automatic Perimetry in Glaucoma: A Practical Guide. Orlando, FL: Grune & Stratton; 1985. Harrington DO, Drake MV. The Visual Fields: A Textbook and Atlas of Clinical Perimetry. 6th ed. St Louis: Mosby; 1989. Lieberman MF. Glaucoma and automated perimetry. Focal Points: Clinical Modules for Ophthalmologists. San Francisco:
American Academy of Ophthalmology; 1993, module 9.
Spry PGD, Johnson CA. Advances in automated perimetry. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2002, module 10.
Walsh TJ, ed. Visual Fields: Examination and Interpretation. 2nd ed. Ophthalmology Monograph 3. San Francisco: American Academy of Ophthalmology; 1996.
Patterns of Glaucomatous Nerve Loss
The hallmark defect of glaucoma is the nerve fiber bundle defect that results from damage at the optic nerve head. The pattern of nerve fibers in the retinal area served by the damaged nerve fiber bundle will correspond to the specific defect. The common names for the classic visual field defects are derived from their appearance as plotted on a kinetic visual field chart. In static perimetry, however, the sample points are in a grid pattern, and the representation of visual field defects on a static perimetry chart generally lacks the smooth contours suggested by such terms as arcuate.
Glaucomatous visual field defects include the following:
generalized depression paracentral scotoma (Fig 3-29)
arcuate or Bjerrum scotoma (Fig 3-30) nasal step (Fig 3-31)
altitudinal defect (Fig 3-32) temporal wedge
Figure 3-29 A paracentral scotoma is an island of relative or absolute vision loss within 10° of fixation. Loss of nerve fibers from the inferior pole, originating from the inferotemporal retina, resulted in the superonasal scotoma shown. Paracentral scotomata may be single, as in this case, or multiple, and they may occur as isolated findings or may be associated with other early defects (Humphrey 24-2 program).
Figure 3-30 An arcuate scotoma occurs in the area 10°–20° from fixation. Glaucomatous damage to a nerve fiber bundle
containing axons from both the inferonasal and inferotemporal retina resulted in the arcuate defect shown. The scotoma often begins as a single area of relative loss, which then becomes larger, deeper, and multifocal. In its full form an arcuate scotoma arches from the blind spot and ends at the nasal raphe, becoming wider and closer to fixation on the nasal side
(Humphrey 24-2 program). (Visual field courtesy of G. A. Cioffi, MD.)
Figure 3-31 A nasal step is a relative depression of one horizontal hemifield compared with the other. Damage to superior nerve fibers serving the superotemporal retina beyond the paracentral area resulted in this nasal step. In kinetic perimetry the nasal step is defined as a discontinuity or depression in one or more nasal isopters near the horizontal raphe (Humphrey 24-
2 program). (Visual field courtesy of G. A. Cioffi, MD.)
Figure 3-32 Altitudinal defect with near complete loss of the superior visual field, characteristic of moderate to advanced glaucomatous optic neuropathy (left eye). (Visual field courtesy of G. A. Cioffi, MD.)
The superior and inferior poles of the optic nerve appear to be most susceptible to glaucomatous damage. However, damage to small, scattered bundles of optic nerve axons commonly produces a generalized decrease in sensitivity, which is harder to recognize than focal defects. Combinations of superior and inferior visual field loss, such as double arcuate scotomata, may occur, resulting in profound peripheral vision loss. Typically, the central island of vision and the inferotemporal visual field are retained until late in the course of glaucomatous optic nerve damage (Fig 3-33).
