- •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
α-Adrenergic agonists
α-Adrenergic agonists lower IOP by both diminishing aqueous production and increasing uveoscleral outflow. The α2-adrenergic agonist brimonidine crosses the blood–brain barrier and therefore has significant effects on the central nervous system. Infants and young children are particularly susceptible to brimonidine’s adverse effects, including apnea, hypotension, bradycardia, hypotonia, hypothermia, and somnolence. α2-Adrenergic agonists are contraindicated in children younger than 3 years. There is some debate about the age at which children can safely use brimonidine. In general, this agent should be used with caution in children between the ages of 3 and 10. The lowest dose should be used and punctal occlusion employed to minimize systemic absorption.
The α-agonist apraclonidine is better tolerated systemically in children, but the risk of follicular conjunctivitis increases with long-term use. Apraclonidine acts as a vasoconstrictor and can be used to minimize bleeding during intraocular surgery.
Prostaglandin analogues
Prostaglandin analogues lower IOP by increasing uveoscleral outflow. They have minimal systemic side effects in children and have been shown to effectively lower IOP in JOAG. They can exacerbate uveitis in postoperative glaucoma patients and should be avoided with uncontrolled uveitis. Their once-daily dosing is helpful for minimizing the stress involved in administering eyedrops to children. Adverse effects include conjunctival hyperemia, hypertrichiasis, periocular pigmentation (reversible), and darkening of irides (permanent) except in blue-eyed patients.
Cholinergic agonists
Cholinergic agonists (miotics) lower IOP by increasing aqueous outflow through the trabecular meshwork. With the newer medications that are available, these agents are rarely used on a long-term basis, but they have a role intraoperatively by inducing miosis, which facilitates angle surgery.
Prognosis and Follow-Up
The long-term prognosis for pediatric glaucoma patients has greatly improved with the development of effective surgical techniques. This is particularly true for PCG patients who are asymptomatic at birth and who present with onset of symptoms between 3 and 12 months of age; IOP can be controlled with angle surgery in approximately 80% of these children. When symptoms are present at birth or when the disease is diagnosed after 12 months of age, the outlook for surgical control of IOP is more guarded.
Pediatric patients whose IOP is controlled by surgery may still experience morbidities related to the previous IOP elevation. These can cause serious lifelong visual compromise and include amblyopia, corneal scarring, strabismus, anisometropia, cataract, lens subluxation, susceptibility to trauma (as occurs in an eye with a thinned sclera), and recurrent glaucoma in the affected or unaffected eye. Clinicians should address these conditions and be prepared to coordinate care with other specialists as needed.
Amblyopia is a common cause of visual compromise, particularly in patients with unilateral glaucoma, corneal opacification, and/or anisometropia. The clinician should aggressively treat amblyopia, addressing conditions contributing to its development, such as refractive error, strabismus, cataract, and corneal clouding. Elevated IOP can lead to buphthalmos in patients with PCG and to progressive myopia and anisometropia in patients with juvenile glaucoma. Haab striae and corneal scarring may cause astigmatism. Refractive errors should be corrected with spectacles, and
use of protective eyewear should be encouraged.
Strabismus may result from glaucoma drainage devices or amblyopia. When performing surgery to correct strabismus, the surgeon should try to minimize conjunctival scarring in anticipation of future glaucoma surgeries and should be cognizant of the sites of prior trabeculectomies and glaucoma drainage device implants.
All cases of childhood glaucoma require lifelong follow-up to monitor IOP and to observe for any complications of prior surgeries and any secondary vision-threatening issues. As relapses of glaucoma may occur even years later, care should be coordinated between glaucoma specialists and pediatric specialists. Educating parents about the need for lifelong care of the child with glaucoma and involving these children in their own care enhance the long-term management of this challenging disease.
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