- •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
CHAPTER 7
Medical Management of Glaucoma
In the management of patients with glaucoma, the ophthalmologist must decide whom, when, and how to treat. This chapter deals largely with the last of these decisions and specifically relates to the medical management of primary open-angle glaucoma (POAG). The major clinical trials on openangle glaucoma have provided an evidence base for the use of medical treatment to lower intraocular pressure (IOP) in glaucoma. These trials are summarized in Chapter 4.
Risk calculators such as the Scoring Tool for Assessing Risk (STAR) and one based on data pooled from the Ocular Hypertension Treatment Study and the European Glaucoma Prevention Study, STAR II, have been used clinically in assessing the risk of glaucoma development in an individual patient with untreated ocular hypertension. The information obtained from these tools can help guide the clinician in deciding which ocular hypertensive patients to treat. These risk calculators are now available for mobile use through smartphone applications.
In patients with established glaucoma, 3 principal factors guide the decision of whether to treat and how aggressively to treat: the life expectancy of the patient, the stage of disease at the time of presentation, and the rate of disease progression. In addition, other factors are taken into consideration, such as the degree of IOP elevation, the presence or absence of optic disc hemorrhages, and the family history.
The stage of disease is important, as a patient who is converting from ocular hypertension to mild glaucoma has a lower risk of significant vision loss compared with a patient who has advanced glaucoma (eg, visual field loss threatening central fixation) at the time of presentation, irrespective of the rate of progression. Likewise, a young patient presenting with glaucoma has a higher risk of vision loss in the long term, because of his or her longer life expectancy, compared with an older patient presenting with the same stage of disease and the same IOP level. Also, a patient demonstrated to have a faster rate of visual field progression has a higher risk of vision loss than one with a slow rate of visual field progression (see Chapter 3 for discussion of visual fields).
The goal of currently available glaucoma therapy is to preserve visual function by lowering IOP to a level that is likely to prevent further optic nerve damage. The treatment regimen chosen should achieve this goal with the lowest risk, fewest adverse effects, and the least amount of disruption to the patient’s life, taking into account the cost of treatment. Although the goal of treatment is to prevent vision loss, current treatments are aimed at lowering IOP and, in the short term, the efficacy of treatment is gauged according to the IOP level. The concept of target pressure was introduced because some patients require lower IOP levels than do others to stabilize their glaucoma. In general, the patients who require lower target pressures are those with more advanced optic neuropathy, although
patients who develop optic nerve damage in the presence of IOP levels that are never elevated also require low target levels.
Despite the significance of the concept of target pressure, it is important not to set a rigid target pressure for the individual patient, as there is no evidence base for doing so. Ideally, the target pressure level should be a broad range (eg, <21 mm Hg, <18 mm Hg, or <15 mm Hg) with an upper IOP limit that is unlikely to lead to further optic nerve damage in a given patient. The range should be individualized for the patient, based on the following: IOP level at which damage is thought to have occurred, severity of the damage, life expectancy of the patient, and associated risk factors.
The more advanced the disease on initial presentation, the lower the target pressure required for preventing further progression in the average patient. Once the optic nerve is damaged, it can incur additional damage more easily. If severe vision loss is already present, then further damage is likely to have a disproportionately greater impact on the patient. An initial IOP reduction of 20% from baseline is a suggested minimum. However, there is no guarantee that reduction of IOP to the target pressure range will prevent disease progression. If further progression does occur, the target pressure range may require revision.
Once the target pressure range has been determined, the clinician must decide how to achieve this goal, medically or surgically. Regardless of which is chosen, the anticipated benefits of any therapeutic regimen should justify the risks, and regimens associated with substantial adverse effects should be reserved for patients with a high probability of progressive vision loss. For example, it may be illogical to expose a patient to the adverse effects of multiple topical medications or oral carbonic anhydrase inhibitors (CAIs) unless significant damage to the visual field and optic nerve has occurred or the IOP is very high.
The interrelationship between medical and surgical therapy is complex, with the choice of treatment varying according to the type of glaucoma. Further, it is not always clear which modality is better. The treatment of angle-closure glaucoma with pupillary block and of primary congenital glaucoma is primarily surgical, either laser or incisional, with medical therapy playing a secondary role. Initial treatment of POAG has commonly been medical, with surgery undertaken only if medical treatment fails or is not well tolerated. The treatment of secondary glaucoma is similar to that of primary glaucoma, with some exceptions, and the underlying cause of the glaucoma should be addressed if possible. However, the Glaucoma Laser Trial (GLT) found that, as initial glaucoma therapy, argon laser trabeculoplasty was at least as effective as medications. The Collaborative Initial Glaucoma Treatment Study (CIGTS) reported that medical therapy was essentially equally as effective as surgical therapy in preventing POAG progression. In fact, with medical therapy, the rate of progression at 5 years was substantially less than had been anticipated. This has been attributed to the definition of progression that was used in the study and to the aggressive IOP lowering obtained in both groups. Surgical therapy is discussed in detail in Chapter 8.
When a patient starts a medication, some clinicians favor using a unilateral treatment trial in order to assess the medication’s efficacy. The continued efficacy of a therapeutic regimen should be reevaluated periodically. To assess a patient’s existing regimen, a reverse therapeutic trial can be performed, which entails stopping a medication in 1 eye, and then comparing the effect in the treated eye with that in the untreated eye.
The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 4. Comparison of treatment outcomes within race: seven-year results. Ophthalmology. 1998;105(7):1146–1164.
The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000;130(4):429–440.
Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701–713.
