- •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
procedures than with cryotherapy. The most common cyclodestructive modalities currently used are transscleral CPC with the diode laser and ECP. CPC is a noninvasive procedure performed transsclerally, whereas ECP is an intraocular procedure in which the laser energy is applied under direct visualization, thereby causing less damage to adjacent tissues. ECP is particularly useful in eyes with distorted anterior segment anatomy and in eyes with prior unsuccessful CPC or cryotherapy. CPC and ECP can be very useful for providing additional IOP lowering after glaucoma drainage device surgery.
Medical Management
Although surgical management is the mainstay of PCG care, medications are frequently required in the treatment of PCG and other childhood glaucomas. Medications can be used to lower IOP before surgery in order to reduce corneal edema and improve visualization during surgery. They may also be used after surgical procedures in order to provide additional IOP lowering. Medical therapy may be useful for forms of childhood glaucoma other than PCG, including JOAG, inflammatory, and aphakic glaucoma and other secondary glaucomas. The safety and efficacy of most FDA-approved glaucoma medications have not been studied in controlled clinical trials specifically in children, although extensive clinical experience guides most clinicians. A full discussion of glaucoma medications can be found in Chapter 7.
β-Adrenergic antagonists
β-Adrenergic antagonists, or β-blockers, decrease aqueous production in the ciliary body and are useful for controlling IOP in children. Topical β-adrenergic antagonists are considered first-line therapy for glaucoma in children. These agents must be used with caution, however, as they have considerable systemic absorption and can cause bronchospasm, bradycardia, and hypotension in susceptible children. β-Blockers should therefore be avoided in children with asthma or significant cardiac disease. To decrease the risk of bronchospasm, the clinician may consider administering the cardioselective β-blocker betaxolol. The risk of adverse effects can also be diminished by occluding the nasolacrimal drainage system for 3 minutes after administration of the medication and by prescribing timolol 0.25% or levobunolol 0.25% instead of the more commonly used 0.5%, particularly in younger children. The clinician should teach parents how to occlude the nasolacrimal drainage system. Patients with lighter irides may respond as well to timolol 0.25% or levobunolol 0.25% as they do to 0.5%.
Carbonic anhydrase inhibitors
Carbonic anhydrase inhibitors (CAIs) decrease IOP by reducing aqueous production. Topical therapy with dorzolamide or brinzolamide has a minimal risk of systemic side effects and is an excellent second-line therapy after the topical β-adrenergic antagonists. There is some concern about the use of topical dorzolamide or brinzolamide in eyes with compromised corneas or after corneal transplantation, although these contraindications are not absolute. Systemic CAIs (acetazolamide and methazolamide) provide slightly more IOP lowering than do the topical preparations, but they have numerous systemic side effects. The pediatric dosage of acetazolamide is 10–20 mg/kg/day. CAIs should not be used in patients with known serious sulfa allergies. Adverse effects include anorexia, diarrhea, weight loss, tingling of the perioral areas and fingers, hypokalemia, and metabolic acidosis; children using diuretics are particularly at risk of experiencing these effects. Because of the risk of these adverse effects and of rare but life-threatening reactions such as Stevens-Johnson syndrome and aplastic anemia, systemic CAIs are reserved for patients at high risk of vision loss due to glaucoma.
