- •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 1-1 Diagrammatic cross section of the anterior segment of the normal eye, showing the site of aqueous production (ciliary body), sites of conventional aqueous outflow (trabecular meshwork–Schlemm canal system and episcleral venous plexus), and the uveoscleral outflow pathway (green arrow). Small white arrow shows normal path of outflow and indicates that resistance in this illustration is relative, not total. (Illustration by Cyndie C. H. Wooley.)
In most individuals with glaucoma, the optic nerve and visual field changes seen with this disease are determined by both the level of the IOP and the resistance of the optic nerve to damage. Although progressive changes in the visual field and optic nerve are often related to elevated IOP, in some glaucoma patients the IOP remains within statistically normal range (see Chapter 4). However, when considering whether glaucomatous damage is truly occurring in a patient with “normal” IOP, the ophthalmologist should take into account the measurement artifact that is caused by variation in central corneal thickness and that occurs with diurnal variation in IOP. In most cases of glaucoma, it is presumed that the IOP is too high for proper functioning of the optic nerve axons and that lowering the IOP will stabilize the damage. In cases involving other pathophysiologic mechanisms that may affect the optic nerve, however, the optic nerve may continue to be damaged despite lowering the IOP.
Preperimetric glaucoma is a term that is sometimes used to denote glaucomatous changes in the optic disc in patients with normal visual fields, as determined by white-on-white perimetry. Accurate diagnosis of this condition depends on the sensitivity of the visual function test that is used. Thus, the development of new, more sensitive tests may allow earlier confirmation of this form of glaucoma, while the patient is within this preperimetric phase.
Classification
Open-Angle, Angle-Closure, Primary, and Secondary Glaucomas
Traditionally, glaucoma has been classified as open angle or closed angle and as primary or secondary (Table 1-1). Differentiating open-angle glaucoma from closed-angle glaucoma is essential from a therapeutic standpoint (Figs 1-2, 1-3), and each type of glaucoma is discussed in detail in Chapters 4 and 5. The concept of primary and secondary glaucomas is also useful, but it reflects our lack of understanding of the pathophysiologic mechanisms underlying the glaucomatous process. There are separate anatomical, gonioscopic, biochemical, molecular, and genetic views of the classification of the glaucomas, among others, each with its own merit. Traditionally, open-angle glaucoma is classified as primary when there is no identifiable underlying anatomical cause of the events that led to obstruction of aqueous outflow and subsequent elevation of IOP (see Fig 1-2). The etiology of the outflow obstruction is generally thought to be an abnormality in the extracellular matrix of the trabecular meshwork and in trabecular cells in the juxtacanalicular region, although other views exist. Trabecular cells and their surrounding extracellular matrix are understood in fairly specific terms, and the basic scientific understanding of the outflow structures is constantly increasing. Glaucoma is traditionally classified as secondary when an abnormality is identified and a putative role in the pathogenesis can be ascribed to this abnormality. As knowledge of the mechanisms underlying the causes of glaucoma has grown, the primary/secondary classification has become increasingly artificial.
Other schemes for classifying glaucoma have been proposed. Classification of the glaucomas based on initial events and classification based on mechanisms of outflow obstruction are 2 schemes that have gained increasing popularity (Table 1-2).
Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. St Louis: Mosby; 1996:722.
Figure 1-2 Schematic of open-angle glaucoma with resistance to aqueous outflow through the trabecular meshwork– Schlemm canal system in the absence of gross anatomical obstruction. (Illustration by Cyndie C. H. Wooley.)
Figure 1-3 Schematic of angle-closure glaucoma with pupillary block leading to peripheral iris obstruction of the trabecular
meshwork. (Illustration by Cyndie C. H. Wooley.)
Table 1-1
