- •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
fibers of the lens to relax, allowing the lens–iris interface to move forward. Furthermore, their use results in an increase in the amount of iris–lens contact, thus potentially increasing pupillary block. For these reasons, miotics, especially the cholinesterase inhibitors, may induce or aggravate angle closure. Gonioscopy should be repeated soon after miotic drugs are administered to patients with narrow angles.
Because of their potential for precipitating angle closure in susceptible individuals, a number of systemic medications that possess adrenergic (sympathomimetic) or anticholinergic (parasympatholytic) activity carry warnings against use by patients with glaucoma; these include allergy and cold medications, antidepressants, and some urological drugs. Although systemic administration generally does not raise intraocular drug levels to the same degree as does topical administration, even slight mydriasis in a patient with a critically narrow chamber angle can induce angle closure. When such drugs are administered to patients with potentially occludable angles, the ophthalmologist should consider informing the patients of this risk and performing iridotomy.
Dapiprazole and thymoxamine are α-receptor blockers that reverse pharmacologic dilation more rapidly than does placebo. Although the use of dapiprazole following pupillary dilation does not eliminate the possibility of precipitating angle closure, it does reduce the overall time that the pupil is dilated, as well as the critical period when the pupil is mid-dilated. Dapiprazole is no longer available in the United States.
Foster PJ, Devereux JG, Alsbirk PH, et al. Detection of gonioscopically occludable angles and primary angle-closure glaucoma by estimation of limbal chamber depth in Asians: modified grading scheme. Br J Ophthalmol. 2000;84(2):186–192.
Plateau Iris
Plateau iris represents an atypical configuration of the anterior chamber angle that may result in acute or chronic ACG. Angle closure in plateau iris is most often caused by anteriorly positioned ciliary processes that critically narrow the anterior chamber recess by pushing the peripheral iris forward. More recent evidence suggests that plateau iris configuration may result from a more anterior junction of the iris dilator muscle and the ciliary epithelium, which causes the iris root to be more articulated. A component of pupillary block is often present. The angle may be further compromised following dilation of the pupil as the peripheral iris bunches up and obstructs the trabecular meshwork. Plateau iris may be suspected if the central anterior chamber appears to be of normal depth and the iris plane appears to be rather flat for an eye with angle closure. This suspicion can be confirmed with gonioscopy or by the presence of the “double hump” sign on ultrasound biomicroscopy. The diagnosis of plateau iris can only be made by gonioscopy or another technique for imaging the angle. The condition will be missed if the examiner relies solely on the slit-lamp examination or the Van Herick method of angle examination.
