- •Foreword
- •Preface
- •List of Contributors
- •Acknowledgments
- •Dedication
- •In Memorium
- •DEFINITIONS
- •EPIDEMIOLOGIC AND SOCIOECONOMIC ASPECTS OF THE GLAUCOMAS
- •RISK FACTORS
- •CLASSIFICATION OF THE GLAUCOMAS
- •REFERENCES
- •Aqueous humor formation
- •FUNCTION OF AQUEOUS HUMOR
- •ANATOMY OF THE CILIARY BODY
- •STRUCTURE
- •ULTRASTRUCTURE OF THE CILIARY PROCESSES
- •VASCULAR SUPPLY
- •MECHANISM OF AQUEOUS FORMATION
- •ULTRAFILTRATION
- •ACTIVE TRANSPORT
- •DIFFUSION
- •CHEMICAL COMPOSITION OF THE AQUEOUS HUMOR
- •THE BLOOD–AQUEOUS BARRIER
- •PRESSURE-DEPENDENT TECHNIQUES
- •Tonography
- •Suction cup
- •Perfusion
- •TRACER METHODS
- •Photogrammetry
- •Radiolabeled isotopes
- •Fluorescein
- •Fluoresceinated dextrans
- •Paraminohippurate
- •Iodide
- •FACTORS AFFECTING AQUEOUS HUMOR FORMATION
- •DIURNAL VARIATION
- •INTRAOCULAR PRESSURE/PSEUDOFACILITY
- •BLOOD FLOW TO THE CILIARY BODY
- •NEURAL CONTROL
- •HORMONAL EFFECTS
- •INTRACELLULAR REGULATORS
- •CLINICAL ASPECTS OF AQUEOUS HUMOR FORMATION
- •CLINICAL CONDITIONS
- •PHARMACOLOGIC AGENTS
- •SURGERY
- •REFERENCES
- •PHYSIOLOGY ISSUES UNIQUE TO THE CONVENTIONAL AQUEOUS OUTFLOW SYSTEM
- •FUNCTIONS OF THE CONVENTIONAL AQUEOUS OUTFLOW SYSTEM
- •ANATOMY OF THE CONVENTIONAL OUTFLOW SYSTEM
- •SCHWALBE’S LINE
- •SCLERAL SPUR
- •TRABECULAR MESHWORK TISSUES
- •Uveal meshwork
- •Corneoscleral meshwork
- •Uveal and corneoscleral meshwork ultrastructure
- •Juxtacanalicular space and cells
- •SCHLEMM’S CANAL
- •Overview
- •Schlemm’s canal inner wall endothelium
- •Glycocalyx
- •Distending cells that form invaginations or pseudovacuoles, ‘giant vacuoles’
- •Schlemm’s canal endothelium pores
- •Sonderman’s canals invaginate into the trabecular meshwork
- •Septa
- •Schlemm’s canal valves spanning across Schlemm’s canal
- •Herniations or protrusions of Schlemm’s canal inner wall
- •Collector channels, aqueous veins and episcleral veins
- •RESISTANCE SITES IN THE AQUEOUS OUTFLOW SYSTEM
- •JUXTACANALICULAR SPACE RESISTANCE
- •SCHLEMM’S CANAL ENDOTHELIUM RESISTANCE
- •PRINCIPLES OF BIOMECHANICS AS A METHODOLOGY TO IDENTIFY TISSUE RESISTANCE
- •TISSUE LOADING STUDIES
- •BOUNDARY CONDITIONS
- •EVIDENCE FROM EXPERIMENTAL MICROSURGERY
- •AQUEOUS OUTFLOW PHYSIOLOGY: PASSIVE AND DYNAMIC FLOW MODELS
- •THE AQUEOUS OUTFLOW SYSTEM AS A PASSIVE FILTER
- •THE AQUEOUS OUTFLOW SYSTEM AS A DYNAMIC MECHANICAL PUMP
- •EXTRINSIC PRESSURE REGULATION MECHANISMS
- •UVEOSCLERAL FLOW
- •METHODS FOR MEASURING FACILITY OF OUTFLOW
- •FACILITY OF OUTFLOW CALCULATIONS
- •Tonography
- •Perfusion
- •Suction cup
- •FACILITY OF OUTFLOW AND ITS CLINICAL IMPLICATIONS
- •FACTORS AFFECTING THE FACILITY OF OUTFLOW
- •HORMONES
- •CILIARY MUSCLE TONE
- •DRUGS
- •SURGICAL THERAPY
- •DIURNAL FLUCTUATION
- •GLAUCOMA
- •EPISCLERAL VENOUS PRESSURE
- •REFERENCES
- •Intraocular pressure
- •INSTRUMENTS FOR MEASURING INTRAOCULAR PRESSURE
- •APPLANATION INSTRUMENTS
- •Goldmann tonometer
- •Perkins tonometer
- •Draeger tonometer
- •MacKay-Marg and Tono-Pen™ tonometers
- •Pneumatic tonometer
- •Non-contact tonometer
- •The Ocuton™ tonometer
- •Maklakow tonometer
- •INDENTATION INSTRUMENTS
- •Schiøtz tonometer
- •Electronic Schiøtz tonometer
- •Impact–rebound tonometer
- •Transpalpebral tonometry
- •DYNAMIC CONTOUR TONOMETRY
- •CONTINUOUS MONITORING OF INTRAOCULAR PRESSURE
- •SUMMARY OF TONOMETRY
- •DISTRIBUTION OF INTRAOCULAR PRESSURE IN THE GENERAL POPULATION
- •FACTORS THAT INFLUENCE INTRAOCULAR PRESSURE
- •RACE
- •HEREDITY
- •DIURNAL VARIATION
- •SEASONAL VARIATION
- •CARDIOVASCULAR FACTORS
- •EXERCISE
- •WIND INSTRUMENT PLAYING
- •LIFESTYLE
- •POSTURAL CHANGES
- •NEURAL FACTORS
- •PSYCHIATRIC DISORDERS
- •HORMONAL FACTORS
- •REFRACTIVE ERROR
- •FOODS AND DRUGS
- •MISCELLANEOUS
- •EYE MOVEMENTS
- •EYELID CLOSURE
- •INFLAMMATION
- •SURGERY
- •REFERENCES
- •Gonioscopic anatomy
- •GROSS ANATOMY
- •ANATOMIC FEATURES OF NORMAL EYES
- •GONIOSCOPIC ANATOMY AND MICROSCOPIC INTERPRETATION
- •PUPIL AND IRIS
- •CILIARY BODY, IRIS PROCESSES, AND SYNECHIAE
- •SCLERAL SPUR
- •SCHWALBE’S LINE
- •TRABECULAR MESHWORK AND TRABECULAR PIGMENT BAND
- •GONIOSCOPIC APPEARANCE
- •REFERENCES
- •Methods of gonioscopy
- •DEFINITION
- •METHODS OF GONIOSCOPY
- •EQUIPMENT
- •Goldmann and Zeiss lenses (indirect method)
- •Koeppe lens (direct method)
- •TECHNIQUE
- •Indirect gonioscopic lenses
- •Indentation (compression) gonioscopy
- •Direct gonioscopic lens
- •REFERENCES
- •GRADING OF CHAMBER ANGLE
- •DIAGRAMMING ANGLE WIDTH, SYNECHIAE, AND PIGMENTATION
- •TRABECULAR PIGMENT BAND
- •SPAETH CLASSIFICATION
- •STEP 4: TRABECULAR MESHWORK PIGMENTATION
- •EXAMPLES
- •DIFFICULTIES AND ARTIFACTS IN GONIOSCOPY
- •CLINICAL USEFULNESS OF GONIOSCOPY
- •AID IN DIAGNOSIS OF TYPE OF GLAUCOMA
- •EVALUATION OF SYMPTOMS
- •USE OF DRUGS
- •POSTOPERATIVE EXAMINATIONS
- •CONDITIONS OTHER THAN GLAUCOMA
- •SUMMARY OF IMPORTANT GONIOSCOPIC TECHNIQUES
- •REFERENCES
- •APPENDIX
- •Visual field theory and methods
- •THE NORMAL VISUAL FIELD
- •VISUAL ACUITY VERSUS VISUAL FIELD
- •TERMINOLOGY AND DEFINITIONS
- •THEORY OF VISUAL FIELD TESTING
- •KINETIC PERIMETRY
- •STATIC PERIMETRY
- •THRESHOLD-RELATED TESTING
- •ZONE TESTING
- •SCREENING TESTS
- •OTHER STATIC TESTING TECHNIQUES
- •THE FUTURE OF VISUAL FIELD TESTING
- •COMBINED STATIC AND KINETIC PERIMETRY
- •REFERENCES
- •PATIENT VARIABLES
- •FIXATION
- •RELIABILITY
- •OCULAR VARIABLES
- •PUPIL SIZE
- •MEDIA CLARITY
- •REFRACTIVE CORRECTION
- •TESTING VARIABLES
- •TECHNICIAN
- •BACKGROUND ILLUMINATION
- •STIMULUS SIZE AND INTENSITY
- •STIMULUS EXPOSURE TIME
- •AREA TESTED
- •EQUIPMENT AND TECHNIQUES
- •GENERAL PRINCIPLES
- •TANGENT SCREEN
- •BOWL PERIMETRY
- •Preparing the patient
- •Technique of computerized bowl perimetry
- •REFERENCES
- •Visual field interpretation
- •GLAUCOMATOUS CHANGES IN THE VISUAL FIELD
- •ANATOMY OF VISUAL FIELD DEFECTS
- •TYPES OF VISUAL FIELD LOSS
- •Generalized loss
- •Localized defects (scotomata)
- •GLAUCOMATOUS VISUAL FIELD DEFECTS
- •Generalized depression
- •Irregularity of the visual field
- •Nasal step or depression
- •Temporal step or depression
- •Enlargement of the blind spot
- •Isolated paracentral scotomata
- •Arcuate defects (nerve fiber bundle defects)
- •End-stage defects
- •Central and temporal islands
- •Reversal of visual field defects
- •ANALYSIS OF VISUAL FIELD LOSS
- •CHRONIC OPEN-ANGLE GLAUCOMA
- •ANGLE-CLOSURE GLAUCOMA
- •OTHER CAUSES
- •ESTERMAN DISABILITY RATING
- •ANALYSIS OF COMPUTERIZED STATIC PERIMETRY
- •RELIABILITY INDEXES
- •False-positive and false-negative responses
- •Fixation reliability
- •FLUCTUATION
- •Short-term fluctuation
- •Long-term fluctuation
- •GLOBAL INDEXES
- •Mean sensitivity
- •Mean deviation or defect
- •Standard deviation or variance
- •GRAPHIC PLOTS
- •AREA OF THE VISUAL FIELD TO BE TESTED
- •LONG-TERM ANALYSIS
- •DETERMINATION OF NORMAL VISUAL FIELD
- •DEVIATION FROM NORMAL VALUES
- •Graphic plot of points varying from normal
- •Global indexes
- •Comparison with the other eye
- •Localized variation within the visual field
- •RECOGNITION OF CHANGE
- •QUANTIFYING VISUAL FIELD CHANGE
- •THE FUTURE OF COMPUTERIZED PERIMETRY
- •REFERENCES
- •Other psychophysical tests
- •INTRODUCTION
- •COLOR VISION AND SHORT-WAVELENGTH AUTOMATED PERIMETRY
- •FREQUENCY-DOUBLING PERIMETRY
- •OTHER PSYCHOPHYSICAL TESTS
- •HIGH-PASS RESOLUTION PERIMETRY
- •MOTION DETECTION PERIMETRY
- •ELECTROPHYSIOLOGY
- •The electroretinogram (ERG)
- •The pattern electroretinogram (PERG)
- •The multifocal electroretinogram (mfERG)
- •The multifocal visual-evoked potential (mfVEP)
- •REFERENCES
- •ANATOMY OF THE OPTIC NERVE HEAD
- •WHERE ARE THE GANGLION CELLS INJURED?
- •WHAT INJURES GANGLION CELLS?
- •Ganglion Cell Susceptibility
- •Connective tissue structures within the optic nerve head
- •Vascular nutrition of the optic disc
- •REFERENCES
- •CLINICAL TECHNIQUES OF EVALUATION
- •OPTIC DISC CHANGES IN GLAUCOMA
- •INTRAPAPILLARY DISC CHANGES
- •Optic disc size
- •Optic disc shape
- •Neuroretinal rim size (NRR)
- •Neuroretinal rim shape
- •Optic cup size in relation to optic disc size
- •Optic cup configuration and depth
- •Cup:disc ratios
- •Position of central retinal vessels and branches
- •PERIPAPILLARY DISC CHANGES
- •Optic disc hemorrhages
- •Nerve fiber layer defects
- •Diameter of retinal arterioles
- •Peripapillary choroidal atrophy
- •PATTERNS OF OPTIC NERVE CHANGES AND SUBTYPES OF GLAUCOMA
- •HIGH MYOPIA DISC PATTERN
- •FOCAL NORMAL-PRESSURE PATTERN (FOCAL ISCHEMIC)
- •AGE-RELATED ATROPHIC PRIMARY OPEN-ANGLE GLAUCOMA PATTERN (SENILE SCLEROTIC)
- •JUVENILE OPEN-ANGLE GLAUCOMA PATTERN
- •PRIMARY OPEN-ANGLE GLAUCOMA PATTERN (GENERALIZED ENLARGEMENT)
- •REFERENCES
- •Optic nerve imaging
- •CONFOCAL SCANNING LASER OPHTHALMOSCOPY (CSLO)
- •HEIDELBERG RETINA TOMOGRAPHY (HRT)
- •Components of the HRT report
- •Evaluating scan quality
- •Strengths and limitations
- •New developments
- •Testing from the patient’s perspective
- •OPTICAL COHERENCE TOMOGRAPHY (OCT)
- •DIFFERENT SCANNING MODALITIES
- •Peripapillary scan
- •Macular scan
- •ONH scan
- •Fast scans
- •COMPONENTS OF THE OCT REPORT
- •RNFL thickness average analysis
- •Macular analysis
- •Optic nerve head analysis
- •QUALITY ASSESSMENT
- •STRENGTHS AND LIMITATIONS
- •TESTING FROM THE PATIENT’S PERSPECTIVE
- •LONGITUDINAL EVALUATIONS
- •SCANNING LASER POLARIMETRY
- •Components of the GDX report
- •Quality assessment
- •Strengths and limitations
- •Testing from the patient’s perspective
- •CONCLUSIONS
- •REFERENCES
- •Primary angle-closure glaucoma
- •HISTORICAL REVIEW AND CLASSIFICATIONS
- •CLASSIFICATIONS OF ANGLE-CLOSURE DISEASE
- •TWENTY-FIRST CENTURY CONSENSUS CLASSIFICATION
- •CLARIFICATIONS AND COMMENTARY
- •PRESENTATIONS OF PRIMARY ANGLE-CLOSURE DISEASE
- •NEW IMAGING TECHNOLOGIES
- •CLASSIFICATION BY MECHANISMS IN THE ANTERIOR SEGMENT
- •PUPILLARY BLOCK GLAUCOMA
- •Epidemiologic studies
- •Demographic risk factors
- •Gender
- •Heredity
- •Refractive error
- •Miscellaneous factors
- •Ocular risk factors and mechanisms
- •Iris bowing and lens–iris channel
- •Provocative tests
- •Clinical presentations of acute PACG with pupillary block
- •Signs and symptoms
- •Clinical examination
- •Treatment of acute PACG
- •Medical management of acute PACG
- •Slit-lamp maneuvers in management of acute PACG
- •Laser interventions for acute PACG
- •Surgical management of PACG
- •Management of the fellow eye
- •Sequelae of acute PACG
- •Correlating older and newer terminologies for angle closure
- •PLATEAU IRIS
- •Plateau iris configuration
- •Plateau iris syndrome
- •Pseudoplateau iris (cysts of the iris and ciliary body)
- •PHACOMORPHIC GLAUCOMA
- •Intumescent and swollen lens
- •REFERENCES
- •OVERVIEW OF TERMS AND MECHANISMS
- •ANTERIOR PULLING MECHANISM
- •NEOVASCULAR GLAUCOMA
- •Histopathology
- •Pathogenesis
- •Conditions and diseases commonly associated with neovascular glaucoma
- •Diabetes mellitus
- •Central retinal vein occlusion
- •Carotid occlusive disease
- •Ocular ischemic syndrome
- •Central retinal artery occlusion
- •Miscellaneous
- •Clinical presentation
- •Treatment
- •IRIDOCORNEAL ENDOTHELIAL SYNDROME
- •Histopathology
- •Pathogenesis
- •Clinical presentation
- •Progressive (essential) iris atrophy
- •Chandler’s syndrome
- •Cogan-Reese syndrome
- •Treatment
- •POSTERIOR POLYMORPHOUS DYSTROPHY
- •Histopathology
- •Pathogenesis
- •Clinical presentation
- •Treatment
- •EPITHELIAL DOWNGROWTH
- •Pathophysiology
- •Histopathology
- •Clinical presentation
- •Treatment
- •FIBROVASCULAR INGROWTH
- •FLAT ANTERIOR CHAMBER
- •INFLAMMATION
- •PENETRATING KERATOPLASTY
- •IRIDOSCHISIS
- •ANIRIDIA
- •POSTERIOR PUSHING (OR ROTATIONAL) MECHANISM
- •CILIARY BLOCK GLAUCOMA (AQUEOUS MISDIRECTION OR MALIGNANT GLAUCOMA)
- •INTRAOCULAR TUMORS
- •NANOPHTHALMOS
- •SUPRACHOROIDAL HEMORRHAGE
- •POSTERIOR SEGMENT INFLAMMATORY DISEASE
- •Treatment
- •CENTRAL RETINAL VEIN OCCLUSION
- •SCLERAL BUCKLING PROCEDURE
- •PANRETINAL PHOTOCOAGULATION
- •RETINOPATHY OF PREMATURITY
- •PUPILLARY BLOCK MECHANISMS
- •Secondary pupillary block glaucoma: iris–lens adhesions
- •Dislocated and subluxed lens
- •Ectopia lentis
- •Microspherophakia
- •REFERENCES
- •Primary open angle glaucoma
- •EPIDEMIOLOGY
- •PREVALENCE
- •PATHOPHYSIOLOGY
- •DIMINISHED AQUEOUS HUMOR OUTFLOW FACILITY
- •Altered corticosteroid metabolism
- •Dysfunctional adrenergic control
- •Abnormal immunologic processes
- •Oxidative damage
- •Other toxic influences
- •OPTIC NERVE CUPPING AND ATROPHY
- •CLINICAL FEATURES
- •FINDINGS
- •DIFFERENTIAL DIAGNOSIS
- •TREATMENT
- •INDICATIONS
- •GOALS
- •Target pressure
- •TYPES OF TREATMENT
- •PROGNOSIS
- •THE GLAUCOMA SUSPECT AND OCULAR HYPERTENSION
- •EPIDEMIOLOGY OF OCULAR HYPERTENSION
- •RISK FACTORS FOR DEVELOPMENT OF OPEN-ANGLE GLAUCOMA
- •TREATMENT
- •NORMAL-TENSION GLAUCOMA
- •PATHOGENESIS
- •CLINICAL FEATURES
- •DIFFERENTIAL DIAGNOSIS
- •WORK-UP
- •TREATMENT
- •REFERENCES
- •Secondary open angle glaucoma
- •PIGMENTARY GLAUCOMA
- •EXFOLIATION SYNDROME (PSEUDOEXFOLIATION SYNDROME)
- •CORTICOSTEROID GLAUCOMA
- •LENS-INDUCED GLAUCOMA
- •PHACOLYTIC GLAUCOMA
- •LENS-PARTICLE GLAUCOMA
- •PHACOANAPHYLAXIS
- •GLAUCOMA AFTER CATARACT SURGERY
- •GLAUCOMA FROM VISCOELASTIC SUBSTANCES
- •GLAUCOMA WITH PIGMENT DISPERSION FROM INTRAOCULAR LENSES
- •UVEITIS-GLAUCOMA-HYPHEMA SYNDROME
- •GLAUCOMA FROM VITREOUS IN THE ANTERIOR CHAMBER
- •GLAUCOMA AFTER TRAUMA
- •CHEMICAL BURNS
- •ELECTRIC SHOCK
- •RADIATION
- •PENETRATING INJURIES
- •CONTUSION INJURIES
- •GLAUCOMA ASSOCIATED WITH INTRAOCULAR HEMORRHAGE
- •GHOST-CELL GLAUCOMA
- •HEMOLYTIC GLAUCOMA
- •HEMOSIDEROSIS
- •HYPHEMA
- •RETINAL DETACHMENT AND GLAUCOMA
- •SCHWARTZ SYNDROME
- •GLAUCOMA AFTER VITRECTOMY
- •GLAUCOMA WITH UVEITIS
- •FUCHS’ HETEROCHROMIC IRIDOCYCLITIS
- •GLAUCOMATOCYCLITIC CRISIS
- •HERPES SIMPLEX
- •HERPES ZOSTER
- •SARCOIDOSIS
- •JUVENILE RHEUMATOID ARTHRITIS
- •SYPHILIS
- •INTRAOCULAR TUMORS AND GLAUCOMA
- •AMYLOIDOSIS
- •ELEVATED EPISCLERAL VENOUS PRESSURE
- •SUPERIOR VENA CAVA OBSTRUCTIONS
- •THYROID EYE DISEASE
- •ARTERIOVENOUS FISTULAS
- •STURGE-WEBER SYNDROME
- •IDIOPATHIC ELEVATIONS
- •REFERENCES
- •TERMINOLOGY
- •CLASSIFICATION
- •SYNDROME CLASSIFICATION
- •PRIMARY GLAUCOMA
- •CLINICAL ANATOMIC CLASSIFICATION
- •Isolated trabeculodysgenesis
- •Iridodysgenesis
- •Anterior stromal defects
- •Structural iris defects
- •Corneodysgenesis
- •CLINICAL PRESENTATION
- •EXAMINATION
- •Office examination
- •Examination under anesthesia
- •Intraocular pressure measurement
- •Corneal measurements: diameter and central thickness
- •Axial length measurement
- •Gonioscopy
- •Ophthalmoscopy
- •Cycloplegic refraction
- •Systemic evaluation
- •PRIMARY CONGENITAL GLAUCOMA
- •INCIDENCE
- •GENETICS AND HEREDITY
- •PATHOPHYSIOLOGY
- •DIFFERENTIAL DIAGNOSIS
- •Other glaucomas
- •Other causes of corneal enlargement or clouding
- •Other causes of epiphora or photophobia
- •Other optic nerve abnormalities
- •MANAGEMENT
- •Preoperative management
- •Initial surgery
- •Follow-up evaluations
- •Filtering surgery
- •Synthetic drainage devices
- •Cyclodestructive procedures
- •Long-term follow-up, management, and prognosis
- •Late developing primary congenital glaucoma
- •GLAUCOMA ASSOCIATED WITH OTHER CONGENITAL ANOMALIES
- •FAMILIAL HYPOPLASIA OF THE IRIS WITH GLAUCOMA
- •DEVELOPMENTAL GLAUCOMA WITH ANOMALOUS SUPERFICIAL IRIS VESSELS
- •ANIRIDIA
- •STURGE-WEBER SYNDROME (ENCEPHALOFACIAL ANGIOMATOSIS, ENCEPHALOTRIGEMINAL ANGIOMATOSIS)
- •NEUROFIBROMATOSIS (VON RECKLINGHAUSEN’S DISEASE)
- •PIERRE ROBIN AND STICKLER SYNDROMES
- •SKELETAL DYSPLASTIC SYNDROMES
- •CORNEODYSGENESIS
- •Axenfeld’s anomaly
- •Rieger’s anomaly and syndrome
- •PETER’S ANOMALY
- •LOWE SYNDROME (OCULOCEREBRORENAL SYNDROME)
- •MICROCORNEA SYNDROMES
- •RUBELLA
- •CHROMOSOME ABNORMALITIES
- •BROAD THUMB SYNDROME (RUBENSTEIN–TAYBI SYNDROME)
- •SECONDARY GLAUCOMA IN INFANTS
- •PERSISTENT FETAL VASCULATURE (PERSISTENT HYPERPLASITIC PRIMARY VITREOUS)
- •RETINOPATHY OF PREMATURITY (RETROLENTAL FIBROPLASIAS)
- •LENS-RELATED GLAUCOMAS
- •Aphakic pediatric glaucoma
- •Subluxation and pupillary block
- •Marfan syndrome
- •Homocystinuria
- •Spherophakia and pupillary block
- •Weill-Marchesani and GEMSS syndromes
- •TUMORS
- •Retinoblastoma
- •Juvenile xanthogranuloma
- •INFLAMMATION
- •Juvenile rheumatoid arthritis
- •STEROID GLAUCOMA IN CHILDREN
- •NEOVASCULAR GLAUCOMA
- •TRAUMA
- •REFERENCES
- •Genetics of glaucoma
- •BASIC GENETICS
- •GENETIC NOMENCLATURE
- •PRIMARY OPEN-ANGLE, NORMAL-TENSION, AND JUVENILE-ONSET OPEN-ANGLE GLAUCOMA
- •TIGR/MYOCILIN
- •OPTINEURIN
- •OTHER GENES IN OPEN-ANGLE GLAUCOMA
- •EXFOLIATION SYNDROME AND GLAUCOMA
- •GLAUCOMA ASSOCIATED WITH DEVELOPMENTAL DISORDERS
- •PRIMARY CONGENITAL GLAUCOMA
- •AXENFELD-RIEGER ANOMALY
- •ANIRIDIA
- •NAIL PATELLA SYNDROME
- •RENAL TUBULAR ACIDOSIS
- •SUMMARY
- •REFERENCES
- •DIAGNOSIS
- •IDENTIFYING GLAUCOMA SUSPECTS
- •DETERMINING ADEQUACY OF TREATMENT
- •TREATMENT FOLLOW-UP
- •DOCUMENTATION OF PROGRESS
- •PATIENT EDUCATION
- •EFFECTIVE JUDGMENT
- •REFERENCES
- •TARGET PRESSURE
- •MEDICAL THERAPY
- •ADVANTAGES
- •DISADVANTAGES
- •SURGICAL THERAPY
- •ADVANTAGES
- •DISADVANTAGES
- •BASIC PHARMACOLOGY
- •BIOAVAILABILITY OF TOPICAL OCULAR MEDICATION
- •TEAR FILM
- •CORNEAL BARRIERS
- •DRUG FORMULATION
- •DRUG ELIMINATION
- •COMPLIANCE
- •GENERAL SUGGESTIONS FOR MEDICAL TREATMENT OF GLAUCOMA
- •ESTABLISH A TARGET PRESSURE
- •ADJUST THE TREATMENT PROGRAM TO THE PATIENT AND HIS OR HER LIFESTYLE
- •WHEN THERAPY IS INEFFECTIVE, SUBSTITUTE RATHER THAN ADD DRUGS
- •CONTINUALLY MONITOR THE TARGET PRESSURE
- •ASK ABOUT AND MONITOR OCULAR AND SYSTEMIC SIDE EFFECTS
- •SIMPLIFY AND REDUCE TREATMENT WHEN POSSIBLE
- •TEACH PATIENTS THE PROPER TECHNIQUE FOR INSTILLING EYEDROPS
- •PROVIDE WRITTEN INSTRUCTIONS
- •COMMUNICATE WITH THE PATIENT’S FAMILY PHYSICIAN
- •ASK ABOUT PROBLEMS WITH THE MEDICAL REGIMEN
- •CONSIDER DEFAULTING AS AN EXPLANATION FOR THE FAILURE OF MEDICAL TREATMENT
- •EDUCATE PATIENTS ABOUT THEIR ILLNESS AND ITS TREATMENT
- •STOP TREATMENT PERIODICALLY TO DETERMINE CONTINUING EFFECTIVENESS
- •MEASURE INTRAOCULAR PRESSURE AT DIFFERENT TIMES OF THE DAY AND AT DIFFERENT INTERVALS AFTER THE LAST ADMINISTRATION OF MEDICATION
- •RECOMMEND COMPARISON SHOPPING FOR MEDICATIONS
- •SUMMARY
- •REFERENCES
- •Prostaglandins
- •MECHANISM OF ACTION
- •DRUGS IN CLINICAL USE
- •LATANOPROST (XALATAN, PHXA41)
- •BIMATOPROST
- •TRAVOPROST
- •FIXED COMBINATION AGENTS
- •SIDE EFFECTS
- •SUGGESTIONS FOR USE
- •REFERENCES
- •MECHANISM(S) OF ACTION
- •EPINEPHRINE
- •DIPIVEFRIN
- •NOREPINEPHRINE
- •Phenylephrine
- •Clonidine
- •Apraclonidine
- •Brimonidine
- •Isoproterenol
- •Salbutamol
- •Others
- •DOPAMINERGIC AGONISTS
- •ADRENERGIC POTENTIATORS
- •MONOAMINE OXIDASE AND CATECHOL O-METHYLTRANSFERASE INHIBITORS
- •6-HYDROXYDOPAMINE
- •PROTRIPTYLINE
- •GUANETHIDINE (ISMELIN)
- •NONADRENERGIC ACTIVATORS OF ADENYLATE CYCLASE
- •DRUGS IN CLINICAL USE
- •Epinephrine (Eppy, Epinal, Epifrin, and generics)
- •Dipivefrin (Propine and generics)
- •Suggestions for use
- •Side effects
- •Clonidine
- •Prophylaxis in anterior segment laser surgery
- •Argon laser trabeculoplasty
- •Laser iridotomy
- •Nd:YAG laser posterior capsulotomy
- •Management of acute pressure rises
- •Management of open-angle and other chronic glaucomas
- •Combination therapy
- •Side effects
- •Suggestions for use
- •SUMMARY
- •REFERENCES
- •Adrenergic antagonists
- •MECHANISM OF ACTION
- •DRUGS IN CLINICAL USE
- •TIMOLOL MALEATE
- •TIMOLOL HEMIHYDRATE
- •BETAXOLOL
- •LEVOBUNOLOL
- •CARTEOLOL
- •METIPRANOLOL
- •PROPRANOLOL
- •ATENOLOL
- •PINDOLOL
- •NADOLOL
- •METAPROLOL
- •LABETOLOL
- •SUGGESTIONS FOR USE
- •OPEN-ANGLE GLAUCOMA
- •ANGLE-CLOSURE GLAUCOMA
- •SECONDARY GLAUCOMA
- •GLAUCOMA IN CHILDREN
- •BLOOD FLOW AND NEUROPROTECTION
- •SIDE EFFECTS
- •OCULAR
- •SYSTEMIC
- •OTHER ADRENERGIC ANTAGONISTS
- •Thymoxamine
- •Dapiprazole
- •Bunazosin
- •Prazosin
- •Others
- •REFERENCES
- •Carbonic anhydrase inhibitors
- •MECHANISM OF ACTION
- •DIRECT EFFECT ON AQUEOUS HUMOR FORMATION
- •INDIRECT EFFECT ON AQUEOUS HUMOR FORMATION
- •DRUGS IN CLINICAL USE
- •TOPICAL CARBONIC ANHYDRASE INHIBITORS
- •Dorzolamide
- •Brinzolamide
- •SYSTEMIC CARBONIC ANHYDRASE INHIBITORS
- •Acetazolamide
- •Methazolamide
- •Ethoxzolamide
- •Dichlorphenamide
- •SIDE EFFECTS
- •TOPICAL CARBONIC ANHYDRASE INHIBITORS
- •ORAL CARBONIC ANHYDRASE INHIBITORS
- •CONTRAINDICATIONS
- •Acidosis and sickling of red blood cells
- •Other severe symptoms
- •Retinal-choroidal blood flow and neuroprotection
- •SUGGESTIONS FOR USE
- •ANGLE-CLOSURE GLAUCOMA
- •OPEN-ANGLE GLAUCOMA
- •SECONDARY GLAUCOMA
- •INFANTILE AND JUVENILE GLAUCOMA
- •OTHER USES
- •REFERENCES
- •Cholinergic drugs
- •MECHANISMS OF ACTION
- •ANGLE-CLOSURE GLAUCOMA
- •OPEN-ANGLE GLAUCOMA
- •DRUGS IN CLINICAL USE
- •DIRECT-ACTING CHOLINERGIC AGENTS
- •Acetylcholine
- •Pilocarpine
- •Alternative drug delivery systems
- •Methacholine (Mecholyl)
- •Carbachol
- •Aceclidine (Glaucostat)
- •INDIRECT (ANTICHOLINESTERASE) AGENTS
- •Echothiophate iodide (phospholine iodide)
- •Demecarium bromide (Humorsol, Tosmilen)
- •Isoflurophate (Floropryl, di-isopropyl fluorophosphate, Dyflos)
- •Physostigmine (eserine)
- •Neostigmine (prostigmine)
- •SIDE EFFECTS
- •OCULAR
- •SYSTEMIC
- •SUGGESTIONS FOR USE
- •EXAMINATION
- •CONTRAINDICATIONS
- •REFERENCES
- •Hyperosmotic agents
- •MECHANISMS OF ACTION
- •DRUGS IN CLINICAL USE
- •ORAL AGENTS
- •Glycerol
- •Isosorbide
- •Ethyl alcohol
- •INTRAVENOUS AGENTS
- •Mannitol
- •Urea
- •SIDE EFFECTS
- •SUGGESTIONS FOR CLINICAL USE
- •ANGLE-CLOSURE GLAUCOMA
- •SECONDARY GLAUCOMA
- •CILIARY BLOCK (MALIGNANT) GLAUCOMA
- •TOPICAL HYPEROSMOTIC AGENTS
- •OTHER
- •REFERENCES
- •General aspects of laser therapy
- •GENERAL ASPECTS OF LASER THERAPY
- •TISSUE EFFECTS OF LASER
- •THERMAL EFFECTS (PHOTOCOAGULATION, PHOTOVAPORIZATION)
- •PHOTODISRUPTION
- •PHOTOABLATION
- •PHOTOCHEMICAL EFFECTS
- •GENERAL PREPARATION OF THE PATIENT
- •BASIC LASER SAFETY
- •REFERENCES
- •LASER PERIPHERAL IRIDOTOMY
- •INDICATIONS
- •TYPES OF LASER
- •GENERAL PREPARATION
- •ND:YAG LASER IRIDOTOMY
- •ARGON OR SOLID-STATE LASER IRIDOTOMY
- •LIGHT BROWN IRIS
- •Dark brown iris
- •Light blue iris
- •COMPLICATIONS OF LASER IRIDOTOMY
- •Iritis
- •Pressure elevation
- •Cataract
- •Hyphema
- •Corneal epithelial injury
- •Endothelial damage
- •Corneal stroma
- •Failure to perforate
- •Late closure
- •Retinal burn
- •Aphakia and pseudophakia with pupillary block
- •LASER IRIDOPLASTY (GONIOPLASTY)
- •PLATEAU IRIS
- •NANOPHTHALMOS
- •LASERS IN MALIGNANT GLAUCOMA
- •REFERENCES
- •LASER TRABECULOPLASTY
- •HISTORY
- •RESULTS
- •SELECTIVE LASER TRABECULOPLASTY
- •Concept
- •Mechanism
- •Technique
- •Patient preparation
- •Procedure
- •POSTOPERATIVE TREATMENT
- •OUTCOMES
- •CONTRAINDICATIONS
- •AS INITIAL THERAPY
- •PREDICTORS OF OUTCOME
- •APHAKIC AND PSEUDOPHAKIC OPEN-ANGLE GLAUCOMA
- •COMPLICATIONS
- •Intraocular pressure elevation
- •Sustained intraocular pressure increase
- •Hyphema
- •Peripheral anterior synechiae
- •Iritis
- •Uveitis
- •EXCIMER LASER TRABECULOSTOMY
- •Concept
- •Technique
- •Outcomes
- •OTHER LASER SCLEROSTOMY TECHNIQUES
- •REFERENCES
- •CYCLOPHOTOCOAGULATION
- •OTHER LASER PROCEDURES
- •SEVERING OF SUTURES
- •REOPENING FAILED FILTRATION SITES
- •CYCLODIALYSIS AND LASER
- •LASER SYNECHIALYSIS
- •GONIOPHOTOCOAGULATION
- •PHOTOMYDRIASIS (PUPILLOPLASTY)
- •REFERENCES
- •General surgical care
- •THE SURGICAL DECISION
- •PREOPERATIVE CARE
- •INSTRUCTIONS TO THE PATIENT
- •OUTPATIENT VERSUS INPATIENT SURGERY
- •PREOPERATIVE MEDICATIONS
- •OPERATIVE CARE
- •THE OPERATING ROOM
- •ANESTHESIA
- •EQUIPMENT
- •POSTOPERATIVE CARE
- •ACTIVITY
- •MEDICATIONS
- •REFERENCES
- •Glaucoma outflow procedures
- •GENERAL CONSIDERATIONS
- •EXTERNAL FILTRATION SURGERY
- •GUARDED PROCEDURES
- •FULL-THICKNESS PROCEDURES
- •RESULTS OF EXTERNAL FILTRATION SURGERY
- •THE CONJUNCTIVAL FLAP
- •LIMBUS-BASED FLAP
- •FORNIX-BASED FLAP
- •EXCISION OF TENON’S CAPSULE
- •GUARDED FILTRATION PROCEDURE
- •TRABECULECTOMY
- •Indications
- •Standard technique
- •Moorfields Safer Surgery System technique
- •Results
- •Surgical options and modifications
- •Triangular versus rectangular flap
- •Postoperative lasering, adjustment, or release of sutures
- •Wound-healing retardants
- •FULL-THICKNESS FILTRATION PROCEDURES
- •THERMAL SCLEROSTOMY (SCHEIE PROCEDURE)
- •SCLERECTOMY
- •Posterior lip sclerectomy
- •Anterior lip sclerectomy
- •TREPHINATION
- •IRIDENCLEISIS
- •GLAUCOMA DRAINAGE DEVICES
- •THE MOLTENO IMPLANT
- •Techniques
- •SCHOCKET PROCEDURE
- •KRUPIN VALVE AND EX-PRESS IMPLANT
- •AHMED VALVE
- •BAERVELDT IMPLANT
- •RESULTS AND COMPLICATIONS OF DRAINAGE DEVICES
- •REFERENCES
- •CATARACT SURGERY IN THE GLAUCOMATOUS EYE
- •TYPES OF GLAUCOMA AND THEIR INFLUENCE ON CATARACT MANAGEMENT
- •SELECTING THE APPROPRIATE SURGICAL APPROACH
- •SELECTING THE APPROPRIATE PROCEDURE: HISTORICAL CONSIDERATIONS
- •SURGICAL TECHNIQUES FOR COMBINED PROCEDURES
- •GENERAL PREOPERATIVE CONSIDERATIONS
- •SMALL-INCISION COMBINED SURGERY
- •Incision sites
- •Fornix versus limbal conjunctival flap
- •Scleral flap
- •Antimetabolite use
- •Managing the small pupil
- •Phacoemulsification techniques
- •Intraocular lens selection
- •Trabeculectomy formation
- •Flap closure
- •Postoperative medical management
- •EXTRACAPSULAR CATARACT EXTRACTION COMBINED SURGERY
- •Miotic pupil
- •Incision construction
- •CATARACT SURGERY WITH PRE-EXISTING FILTRATION BLEB
- •REFERENCES
- •BUTTONHOLING THE CONJUNCTIVA
- •THE SHALLOW AND FLAT ANTERIOR CHAMBER
- •FLAT ANTERIOR CHAMBER WITH HYPOTONY
- •FLAT ANTERIOR CHAMBER IN NORMOTENSIVE AND HYPERTENSIVE EYES
- •CILIARY BLOCK (MALIGNANT GLAUCOMA)
- •SUPRACHOROIDAL HEMORRHAGE (SCH)
- •INTRAOPERATIVE FLAT ANTERIOR CHAMBER
- •HYPHEMA
- •LARGE HYPHEMA
- •INTRAOCULAR INFECTION
- •SYMPATHETIC OPHTHALMIA
- •FILTRATION FAILURE
- •DIGITAL PRESSURE
- •FAILURE DURING THE FIRST POSTOPERATIVE WEEK
- •PLUGGED SCLEROSTOMY SITE
- •RETAINED VISCOELASTIC MATERIAL
- •TIGHT SCLERAL FLAP: RELEASABLE SUTURES AND LASER SUTURE LYSIS
- •INADEQUATE OPENING OF DESCEMET’S MEMBRANE
- •ENCAPSULATED BLEB
- •REOPERATION AFTER FAILED FILTRATION
- •REVISION OF ENCYSTED BLEB
- •Needling of failed blebs
- •Slit-lamp or minor surgery setting
- •Operating room setting
- •FAILED FILTRATION WITH NO BLEB
- •BLEB COMPLICATIONS AND MANAGEMENT
- •THIN-WALLED BLEBS
- •DIFFUSE BLEBS
- •OVERFUNCTIONING BLEBS
- •DELLEN
- •HYPOTONOUS MACULOPATHY
- •LATE HYPOTONY AFTER FILTERING SURGERY
- •HYPOTONY WITH OCCULT FILTERING ‘BLEB’
- •HYPOTONY WITH OCCULT CYCLODIALYSIS CLEFTS
- •HYPOTONY WITH AQUEOUS SUPPRESSION THERAPY IN CONTRALATERAL EYE
- •HYPOTONY FROM RETINAL DETACHMENT
- •HYPOTONY FROM IRITIS OR ISCHEMIA
- •REFERENCES
- •SURGERY FOR INFANTILE AND JUVENILE GLAUCOMA
- •GONIOTOMY
- •Preoperative considerations
- •Intraoperative procedures
- •Complications
- •Practice goniotomy
- •Other ab-interno angle surgery
- •TRABECULOTOMY AB EXTERNO
- •EVALUATION OF GONIOTOMY AND TRABECULOTOMY
- •COMBINED TRABECULOTOMY AND TRABECULECTOMY
- •TRABECULODIALYSIS
- •MISCELLANEOUS PROCEDURES
- •Goniosynechialysis
- •Cyclocryotherapy
- •Retrobulbar alcohol injection
- •Earlier procedures
- •REFERENCES
- •New ideas in glaucoma surgery
- •INTRODUCTION
- •NON-PENETRATING GLAUCOMA SURGERY
- •VISCOCANALOSTOMY
- •BYPASS INTRASCLERAL CHANNELS (NON-PENETRATING DEEP SCLERECTOMY)
- •SHUNTS INTO SCHLEMM’S CANAL
- •TRABECTOME®
- •SHUNTS INTO THE SUPRACHOROIDAL SPACE
- •SUMMARY
- •REFERENCES
- •Challenges for the new century
- •PATHOPHYSIOLOGY
- •CLASSIFICATION AND DIAGNOSIS
- •SCREENING
- •TREATMENT
- •CONCLUSION
- •REFERENCES
- •Appendix
- •GLAUCOMA CONSENSUS
- •GLAUCOMA DIAGNOSIS – STRUCTURE AND FUNCTION (2004)
- •CONSENSUS STATEMENTS
- •Structure
- •Function
- •Function and structure
- •GLAUCOMA SURGERY – OPEN ANGLE GLAUCOMA (2005)
- •CONSENSUS STATEMENTS
- •Indications for glaucoma surgery
- •Argon laser trabeculoplasty
- •Wound healing
- •Trabeculectomy
- •Combined cataract/trabeculectomy
- •Aqueous shunting procedures with glaucoma drainage devices
- •Comparison of procedures: trabeculectomy versus aqueous shunting procedures with glaucoma drainage devices
- •Non-penetrating glaucoma drainage surgery
- •Comparison of trabeculectomy with non-penetrating drainage glaucoma surgery in open-angle glaucoma
- •Cyclodestruction
- •Comparison of cyclophotocoagulation and glaucoma drainage device implantation
- •ANGLE CLOSURE AND ANGLE-CLOSURE GLAUCOMA (2006)
- •CONSENSUS STATEMENTS
- •Management of acute angle closure crisis
- •Surgical management of primary angle-closure glaucoma
- •Laser and medical treatment of primary angle-closure glaucoma
- •Laser and medical treatment of primary angle-closure glaucoma
- •Detection of primary angle closure and angle-closure glaucoma
- •INTRAOCULAR PRESSURE (2007)
- •CONSENSUS STATEMENTS
- •Measurement of intraocular pressure
- •Intraocular pressure as a risk factor for glaucoma development & progression
- •Epidemiology of intraocular pressure
- •Clinical trials and intraocular pressure
- •Target intraocular pressure in clinical practice
- •Index
part
4 Clinical entities
Rarely, acute attacks persist despite a patent iridotomy, nearly always necessitating surgery for cataract extraction and/or filtration.70
Argon and Nd:YAG iridotomies have virtually replaced surgi-
cal iridectomy as the preferred technique for performing iridec- tomy.245–251 The term iridotomy is used to indicate laser-induced
openings in the iris, whereas iridectomy indicates surgical removal of iris tissue. Although surgical iridectomy is a relatively safe and simple procedure, it is invasive and presents a small but still present risk of intraocular complications such as cataract, bleeding, and endophthalmitis. Surgical iridectomy is now reserved for such infrequent situations such as: the laser fails to produce a patent iridotomy; laser iridotomies repeatedly close; a laser is neither available nor functioning properly; opacities of the cornea interfere with laser treat-
ment; or the patient is uncooperative or unable to sit at the slit lamp.194,252–256 Often if the eye comes to filtration, an additional
surgical iridectomy may be advisable.
Argon laser iridotomies, in contrast to those performed with a Nd:YAG laser, may close at a later date, subjecting the eye to redevelopment of angle closure.257 Closure of laser iridotomies is usually by regrowth of iris pigment epithelium.258 Fleck257 has calculated that a 15- m opening is theoretically large enough to prevent pupillary block; however, localized iris edema, pigment epithelial proliferation, and changes in iridotomy size after pupil dilation may obstruct a small opening.Therefore it is recommended that an iridotomy between 150 and 200 m should be created.
If an acute attack can be terminated by medical means, the physician can proceed directly to laser iridotomy, or wait 1–2 days for the cornea to clear and intraocular inflammation to subside. The physician must observe the IOP and the patient carefully to ensure that a repeat attack does not occur.
Laser iridoplasty (gonioplasty) and pupilloplasty As mentioned above and addressed in Chapter 31, other argon laser interventions have their role in the management of acute PACG. The peripheral iridoplasty (also referred to as gonioplasty) is a viable treatment in three settings: (1) acute PACG from pupillary block, unresponsive to medical treatment, and where a perforating laser iridotomy is precluded by excessive shallowing of the anterior chamber, inflammation or corneal edema; (2) plateau iris syndrome; and (3) acute phacomorphic angle closure. Though easiest to perform in areas
free of PAS, iridoplasty is remarkably effective in the management of acute angle closure, with either 180° or 360° of treatment.259,260
This technique has proven to be as effective as intensive medical therapy with pilocarpine, timolol, and acetazolamide.241
The role of iridoplasty in managing angle-closure disease caused by plateau iris is discussed more fully below. In brief, by itself it
is effective in opening the angle, sometimes for the long term; when combined with, or after,261–264 a laser iridotomy, it may well
serve as an effective treatment for this condition.265 As mentioned, pupilloplasty refers to laser techniques which can interrupt pupillary block by distorting the pupil into a tear-shaped configuration, focally interrupting decreased flow through the iris–lenticular junction, thus facilitating aqueous egress into the anterior chamber. Both techniques are important components of the laser armamentarium in managing acute angle-closure disease.
Surgical management of PACG
There are slightly different considerations for surgical intervention for the acute and the long-term manifestations of PACG. If IOP elevation persists despite a patent laser iridotomy in acute disease and subsequent medical therapy, there are several compelling surgical options that have been proffered, but not yet universally
embraced: filtering surgery alone; lens extraction alone, with or without goniosynechialysis; combined lens extraction with trabeculectomy; or goniosynechialysis alone.266–268 Often pressure reduction is the primary focus in this context, with surgery often made challenging by persistently elevated IOPs, diminished corneal clarity, shallow anterior chamber, and inflammation accompanying the acute crisis. Surgical goals for chronic PACG are comparable to the considerations for operating in eyes with uncontrolled POAG: long-term IOP reduction towards a target range, stabilization of progressive disc and/or visual field deterioration, and addressing the juxtaposition of cataractous visual loss in conjunction with the need for glaucoma surgery. However, most of these procedures have not been evaluated for PACG in a randomized controlled fashion with different populations, and the literature must be approached with caution.
Trabeculectomy with and without antimetabolite seem to be equally valid approaches.269–271 One major center in the study of
PACG reported a significantly higher rate of trabeculectomy failure (over one-third of cases) and complications in medically uncontrolled PACG eyes than in eyes which were medically controlled, suggesting that filtration surgery may not be the ‘procedure of choice’ in such circumstances.272 Neverthless, acute PACG eyes in
both Asia and the US require filtering surgery between one-third and one-half of the time.273
Because of the causative role of a large, anteriorly located lens in pupillary block,174 lens removal and intraocular lens (IOL) implantation is an attractive primary surgical approach: it offers the patient the likelihood of improved vision, and it is a technique that is familiar to many more surgeons throughout the world than is trabeculectomy.Although it has been recommended as a primary intervention274 and appears capable of restoring angle anatomy to a more normal configuration,275 it nevertheless can be a daunting operative procedure in the semi-acute setting, confronting the surgeon with such challenges as a shallow anterior chamber, a convex lens prone to anterior capsular tears, and a flacid iris from ischemic damage.268 A particularly exciting and well-controlled study found phacoemulsification/IOL surgery to be comparable to, and in fact more advantageous than, laser iridotomy in the management of acute PACG.223 The applicability of this approach among different populations and its long-term safety and efficacy in the hands of surgeons with various techniques and skill levels remain to be clarified.
The combination procedures of cataract with filtration surgery,276 or cataract with glaucoma shunt have also been described in the contect of PACG management.277 But in the absence of data as to the advantages or disadvantages of a one-stage combined versus twostage procedure for coexistent uncontrolled acute PACG with cataract, the decision as to which approach to follow remains subjective.
Goniosynechialyis refers to the deliberate intra-operative shearing
or peeling of synechial adhesions in the angle, either mechanically or with a viscoelastic dissection, for at least 180°.266,267 Originally
proposed by Campbell and Vela as an intervention appropriate for
eyes with PAS documented to be less than a year old, it has since been used in conjunction with cataract surgery.278,279 The proce-
dure’s duration of effectiveness is, however, unclear, with UBM studies documenting only a short-term effect of opening the angle.280
Management of the fellow eye
Fellow eyes of an eye presenting with acute PACG require a laser iridotomy. Implicit in the three-stage classification of PAC disease is the clinical reality that many eyes steadily progress through the natural history of the condition, unless that course is interrupted. Although it appears there is considerable ethnic variation among
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Primary angle-closure glaucoma |
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the rates of disease progression – with Caucasian eyes showing slow
conversion to complete angle closure, sometimes after more than 25 or 30 years,192,281–288 in contrast to Mongolian and Chinese eyes
suffering rapid development of disease289 – it is important to consider a presenting eye in terms of its stage-specific manifestations.
Eyes identified in the early stages of either demonstrating iridotrabecular touch without elevated IOPs (PAC suspects), are less likely than eyes with elevated IOPs and/or PAS yet normal discs and fields (PAC), to benefit from early laser iridotomies.227 But, as discussed above, we still await long-term controlled studies of specific populations to determine how tight the criteria for angle embarrassment needs to be to obtain maximum benefit from early iridotomies with an acceptably low rate of complications. Elevated IOP is of course seen more commonly in eyes the greater the PAS. However, increased IOP is also found in eyes without synechiae, suggesting that transient apposition between the iris and trabecular meshwork can chronically damage the outflow channels, as histologically demonstrated by Sihota and colleagues.45 Again the clinical conclusion is the necessity of vigorous surveillance, with periodic gonioscopic, disc, and field assessments.
In contrast, at the other end of the disease spectrum are PACG eyes with demonstrable glaucomatous damage to the disc and field, which by and large require laser iridotomy to eliminate the component of pupillary block; yet such an intervention is not always sufficient to completely manage the glaucomatous process, especially in Asian populations.149 Whether early phacoemulsification/IOL surgery is a viable alternative to laser iridotomy for managing the eye with glaucomatous damage has not been completely determined.
As emphasized previously, miotics alone are not considered an appropriate prophylactic measure to forestall PAC progression, since they don’t reliably prevent, and may in fact precipitate, acute attacks. Their chronic administration may exacerbate the development of PAS, cataracts, and conjunctival changes detrimental to successful filtration surgery. Similarly, there is no evidence to support the reliability of provocative tests in predicting which eyes are at risk of progression or need intervention.
Sequelae of acute PACG
In the early post-iridotomy period, elevated IOP may occur as a result of release of pigment and other debris, incomplete or sealed iridotomy, unrecognized plateau iris syndrome, inflammation, extensive PAS, or corticosteroid administration.290,291 Elevated IOP can also occur months to years later and has been reported
in 24–72% of eyes following surgical iridectomy for angle-closure glaucoma.194,247,249,252–255 Though these older studies lack the con-
sistent criteria now in use for staging PAC disease, their findings reflect the need for vigorous surveillance. Patients must be explicitly warned of the need for lifelong care even when iridotomy has apparently ‘cured’ their acute glaucoma.
In Chinese patients, over 50% of eyes with acute PACG after iridotomy develop elevated IOPs, most within 6 months.48 Furthermore, as many as 17% of such patients become blind in an eye with an acute attack within 6 or so years; therefore, close monitoring is mandatory, even with successful breaking of the attack and after iridotomy.149 It is commonplace to recognize that once optic nerve damage can be demonstrated after an acute attack – i.e., PACG is manifest – iridotomy won’t sufficiently control pressure, and supplemental medical therapy or surgery is required.47
The treatment of the PACG after iridotomy is similar to that for open-angle glaucoma, with a stepwise escalation of medical therapy and filtering surgery as needed, but with more frequent gonioscopy.
Some researchers have reported that synechial closure may be alleviated by argon laser iridoplasty (gonioplasty), enhancing visuali-
zation of the trabecular meshwork and giving access to perform trabeculoplasty if needed.262–264 However, its long-term effective-
ness for pressure control has not yet been established, with synechiae often reappearing over time.
While typical glaucomatous visual field loss following an acute attack of PACG occurs in the minority of eyes (about 40%), nerve
fiber layer loss can be demonstrated in most patients whose attack’s duration was longer than 48 hours.292–294 The severity of visual
field loss is directly correlated with the level of IOP during the attack.295 The characteristics of field loss after an acute attack vary in different accounts: some report a predilection for broad arcuate damage;296 others note generalized perimetric defects;297 and yet others remark on the vulnerability of the nasal field.298
The development of visually significant cataract is a relatively common occurrence following acute-angle attacks (nearly all of whom were treated with iridotomies), reported in nearly a third of such eyes.149 Cataract rates after surgical iridectomies were even higher.53 The distinction between cause and effect, however, is unclear. Large, cataractous lenses are often a contributor to pupillary block, so many patients already have some lens opacity when the attack occurs. Most investigators believe that surgical iridectomy accelerates the development of lens changes. Although argon laser can produce localized lens changes, no data exist yet to prove laser iridotomy as a cause of generalized lens opacity. A review of patients treated with argon laser peripheral iridotomy showed no statistically significant differences from ageand sex-matched controls in the development or severity of cataract development.51
Corneal damage can occur both from the acute attack itself and, to a limited extent, from the laser iridotomy treatment. A decrease
in central corneal endothelial cell density has been reported following acute attacks of angle-closure glaucoma.54–56 The decrease in
cell density correlates with the duration of the attack; in fact, longer attacks may cause as much as 77% endothelial cell loss.56,86 The loss of
endothelial cells also correlates with other indicators of ocular damage, including visual field loss and optic disc cupping.57 Occasionally corneal decompensation requiring penetrating keratoplasty occurs after an acute attack. Patients with Fuchs’ endothelial dystrophy have shallower anterior chamber depths, shorter axial lengths, and a greater propensity for increased IOP after penetrating keratoplasty.58
At the corneal surface, the argon laser can cause superficial burns, especially if a contact lens is not used during iridotomy; such burns, however, usually disappear within a few days. Deeper but mild endothelial loss after laser iridotomy has been noted.67 The Nd:YAG laser can cause a localized area of denuded cor-
neal endothelial cells, especially if a contact lens is not used59 or if the treated iris is very close to the corneal endothelium.60,61
However, there is usually no generalized decrease in endothelial cell density with clinical sequelae following iridotomy.62–66 However, patients with pre-existing endothelial dystrophy who suffer an acute angle-closure attack may be more susceptible to
the effects of laser iridotomy, developing corneal decompensation after treatment.61,63
Correlating older and newer terminologies for angle closure
The following section is an attempt to accommodate the rich clinical literature of angle-closure disease within the newer structural classification used today. Since the gonioscopic estimation of the
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