- •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 5-3 A, Plateau iris syndrome with a flat iris plane but shallow angle recess (arrow). Note that the midperipheral angle appears deeper (double arrow) than the narrow angles associated with pupillary block. B, Plateau iris syndrome, with a much deeper angle recess (arrow) following laser peripheral iridoplasty. (Courtesy of M. Roy Wilson, MD.)
The initial management of plateau iris includes either laser iridotomy to remove any component of pupillary block or lensectomy if cataract is present. Eyes with plateau iris remain predisposed to angle closure despite a patent iridotomy as a result of the peripheral iris anatomy. Thus, careful assessment of the angle following iridotomy or lensectomy is necessary to determine whether additional treatment to further deepen the angle is required. PAS have been reported to begin at the Schwalbe line and then to extend in a posterior direction over the trabecular meshwork, scleral spur, and angle recess. The reverse is seen in pupillary block–induced angle closure, in which PAS form in the posterior to anterior direction. These patients may be treated with long-term miotic therapy. However, argon laser peripheral iridoplasty may be more useful in individuals with this condition to flatten and thin the peripheral iris (Fig 5-3). Repeated gonioscopy at regular intervals is necessary because the threat of chronic angle closure may remain despite measures to deepen the angle recess.
Pavlin CJ, Foster FS. Plateau iris syndrome: changes in angle opening associated with dark, light, and pilocarpine administration. Am J Ophthalmol. 1999;128(3):288–291.
Secondary Angle Closure With Pupillary Block
Lens-Induced Angle Closure
Phacomorphic glaucoma
The mechanism of phacomorphic glaucoma is typically multifactorial. However, by definition, a significant component of the pathological angle narrowing is related to the acquired mass effect of the cataractous lens itself. As with primary angle closure, pupillary block often plays an important role in this condition. Phacomorphic narrowing of the angle generally occurs slowly with formation of the cataract. However, in some cases, the onset may be acute and rapid, precipitated by marked lens swelling (intumescence) as a result of cataract formation and the development of pupillary block in an eye that is otherwise not anatomically predisposed to closure (Figs 5-4, 5-5). Distinguishing between primary angle closure and phacomorphic angle closure is not always straightforward and may not be necessary since the treatment of both conditions is similar; but disparities between the 2 eyes in ACD, gonioscopy, and degree of cataract should suggest a phacomorphic process (Fig 5-6). (See also BCSC Section 11, Lens and Cataract.) A laser iridotomy followed by cataract extraction in
a quiet eye is the preferred treatment. In many cases, the iridotomy is unnecessary, as cataract surgery is the definitive treatment in eyes that have the potential for improved vision. Cholinergic agents have a minimal role in the treatment of this condition because they may further narrow the angle and worsen the vision in the presence of cataract. Further, the miotic pupil will make subsequent cataract surgery more difficult.
Figure 5-4 Phacomorphic glaucoma. Lens intumescence precipitates pupillary block and secondary angle closure in an eye not anatomically predisposed to angle closure. (Courtesy of Steven T. Simmons, MD.)
Figure 5-5 Phacomorphic glaucoma. A, In this example, the angle remains narrow despite a patent iridotomy. B, In bright light the angle is transiently made deeper by pupil constriction. C, In this case, a more long-term solution is accomplished by
thinning the peripheral iris with argon laser iridoplasty. Lensectomy is also a viable treatment strategy. (Courtesy of Yaniv Barkana,
MD.)
Figure 5-6 Phacomorphic glaucoma often presents clinically as acute angle-closure glaucoma. Disparities in the anterior chamber depths and degree of cataract between the 2 eyes can help the clinician distinguish between a phacomorphic process and primary angle-closure glaucoma. (Courtesy of Steven T. Simmons, MD.)
Ectopia lentis
Ectopia lentis is defined as displacement of the lens from its normal anatomical position (Fig 5-7). With forward displacement, pupillary block may occur, resulting in iris bombé, shallowing of the anterior chamber angle, and secondary angle closure. This may present clinically as an acute event with pain, conjunctival hyperemia, and vision loss, or as a chronic ACG with PAS formation secondary to repeated attacks. Two laser iridotomies 180° apart is the treatment of choice to relieve the pupillary block and temporize until more definitive lensectomy, if indicated from a visual function standpoint. Lens extraction is usually indicated to restore vision and to reduce the risk of recurrence of pupillary block and development of chronic angle closure. See Table 5-2 for a list of conditions that can cause this entity.
Figure 5-7 Ectopia lentis: dislocation of the lens into the anterior chamber through a dilated pupil. (Courtesy of Ron Gross, MD.)
Table 5-2
Microspherophakia, a congenital disorder in which the lens has a spherical or globular shape, may cause ectopia lentis and subsequent pupillary block and ACG (Fig 5-8). Treatment with cycloplegia may tighten the zonule, flatten the lens, and pull it posteriorly, breaking the pupillary block. Miotics may make the condition worse by increasing the pupillary block and by rotating the ciliary body forward, loosening the zonule and allowing the lens to become more globular. Microspherophakia is often familial and may occur as an isolated condition or as part of either Weill-Marchesani or Marfan syndrome. Finally, the most common form of acquired zonular insufficiency and crystalline lens subluxation occurs in the exfoliation syndrome (Fig 5-9).
Figure 5-8 Ectopia lentis. In a case of microspherophakia, the lens (arrow) is trapped anteriorly by the pupil, resulting in iris bombé and a dramatic shallowing of the anterior chamber.
Figure 5-9 The exfoliation syndrome is a common cause of subluxation of the crystalline lens. A, Right eye of patient with complete dislocation of the lens. B, Gonioscopic view of the same eye reveals that the dislocated lens is in the inferior vitreous cavity. C, Left eye of same patient showing subluxation of the lens. (Courtesy of Thomas W. Samuelson, MD.)
Aphakic or pseudophakic angle-closure glaucoma
Pupillary block may occur in aphakic and pseudophakic eyes. An intact vitreous face can block the pupil and/or an iridectomy in aphakic or pseudophakic eyes or in a phakic eye with a dislocated lens. Generally, the anterior chamber shallows and the iris shows considerable bombé configuration. Treatment with mydriatic and cycloplegic agents may restore the aqueous flow through the pupil but may also make performing a laser iridotomy difficult initially. Topical β-adrenergic antagonists, α2- adrenergic agonists, carbonic anhydrase inhibitors, and hyperosmotic agents can be effective in reducing IOP prior to the placement of an iridotomy. One or more laser iridotomies may be required.
A variant of this problem occurs with anterior chamber intraocular lenses. Pupillary block develops with apposition of the iris, vitreous face, and/or lens optic. The lens haptic or vitreous may obstruct the iridectomy or the pupil, and the peripheral iris bows forward around the anterior chamber IOL to occlude the chamber angle. The central chamber remains deep relative to the peripheral chamber in this instance, because the lens haptic and optic prevent the central portions of
