- •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
membrane with cryotherapy after the eye has been filled with air. Yet another approach involves excision of involved tissues, a penetrating keratoplasty, and implantation of a glaucoma shunt.251 One case report using adjunctive 5-fluorouracil, both for glaucoma control and in an attempt to control the epithelialization, was unsuccessful. Many other techniques have been described in the past for treating epithelial ingrowth, including X-radiation, beta-irradiation, curettage with alcohol, and photocoagulation.252–254 These have been largely abandoned as ineffective. Immunotoxin has been shown to inhibit epithelial proliferation in tissue culture;255 perhaps an agent like this may find some use in the future in this very frustrating condition.
All of the current techniques have been reported to salvage some eyes with epithelial downgrowth and even to maintain good vision in a few cases. However, recurrences of the downgrowth are common, and surgery is frequently associated with complications that include corneal edema, chronic inflammation, macular edema, and phthisis bulbi.The results of treatment are better if the condition is diagnosed early. However, it must be stressed that preventing epithelial downgrowth is far more effective than treating established disease. Surgical and traumatic wounds must be cleaned of epithelial tissue fragments and foreign material and then sutured meticulously.
Fibrovascular ingrowth
Fibrovascular tissue can grow into an eye if there is an open wound after penetrating trauma or surgery. Fibrovascular ingrowth occurs more frequently if the trauma or surgery is associated with hemorrhage, inflammation, or incarcerated tissue.256–258 Fibrovascular ingrowth can occur from pars plana incisions, as well as from more anterior ones.259 In some cases the ingrowth resembles a vascular stalk that enters the eye through an old wound and then fans out over the anterior segment. In other cases the ingrowth forms a gray-white membrane posterior to the corneal endothelium, without an obvious entry site or a vascular stalk. The membrane may have an interlacing pattern of gray fibers that has been compared to woven cloth.260 Various authorities have attributed the invading fibroblasts to the subconjunctival connective tissue, corneal stroma, limbal tissue,261 and metaplastic endothelium.262 The invading fibrovascular tissue grows over the corneal endothelium, anterior iris surface, vitreous face, and angle, where it contracts to form PAS. On occasion the membrane can also attach to the retina and cause a traction detachment.
Fibrovascular ingrowth usually causes glaucoma when the membrane covers the angle and then contracts to form peripheral anterior synechiae. Other factors contributing to the glaucoma include uveitis, pupillary block, and underlying trauma. In many ways, fibrovascular ingrowth resembles epithelial downgrowth, although it is less virulent in its course.263
It is far better to prevent fibrovascular ingrowth than to treat the condition once established. In the past this condition was a common finding in eyes enucleated after cataract surgery or trauma.264 With current microsurgical techniques, fibrovascular ingrowth is encountered far less often.
The glaucoma associated with fibrovascular ingrowth is usually managed by medical therapy. In some cases posterior glaucoma drainage device implantation or cyclophotocoagulation is required to control IOP. On occasion it is possible to excise the fibrovascular tissue, including the fistula at the old wound. However, this approach is not suitable for most eyes with fibrovascular ingrowth because the involvement of the anterior segment is too extensive.
Furthermore, the poor visual prognosis usually does not warrant such aggressive surgery in most cases. Cyclodestructive procedures can often alleviate painfully high IOPs.
Glaucoma has been reported from proliferation of iris melanocytes across the angle and the remainder of the anterior segment.265 This type of glaucoma is extremely rare.
Flat anterior chamber
A flat anterior chamber after penetrating trauma or surgery can lead to the formation of PAS and secondary angle-closure glaucoma without pupillary block (Table 16–1; Fig. 16–9). The development of synechiae is related to the duration of the flat anterior chamber and the degree of inflammation of the eye. There are a number of reports on delayed re-formation of the anterior chamber after cataract extraction. In most of these studies secondary
angle-closure glaucoma was common if the anterior chamber was flat for 5 days or longer.267–269 Flat anterior chambers are encoun-
tered far less often with modern microsurgical cataract techniques. However, flat anterior chambers occur not uncommonly after filtering operations, and they are often allowed to persist for a few to several days before re-formation is attempted. Flat anterior chambers also may occur in association with malignant glaucoma and penetrating keratoplasty.
Following re-formation of a flat anterior chamber, the residual secondary angle-closure glaucoma is treated with standard medical therapy. Often patients respond better to medical treatment than would have been predicted by the extent of the angle closure.This suggests that some of the trabecular meshwork is functional behind the apparent PAS; that is, the synechiae are bridging rather than closing the angle if the duration of tissue approximation is short enough. If medical treatment is inadequate, a laser trabeculoplasty can be considered if at least one-third to one-half of the angle is open. However, the clinician must be aware that a sustained postlaser IOP rise may necessitate filtering surgery. Other alternatives include filtering operations, cyclodestructive procedures, and surgical goniosyneechialysis of the PAS.270
Inflammation
Inflammation can produce glaucoma through a variety of mechanisms, including increased viscosity of the aqueous humor, obstruction of the trabecular meshwork by inflammatory cells and debris, scarring of the outflow channels, elevated episcleral venous pressure, forward displacement of the lens–iris diaphragm, and pupillary block from posterior synechiae. Inflammation can also produce angleclosure glaucoma without pupillary block when the peripheral iris swells as a result of the inflammatory process, when precipitates or exudates in the angle contract to form PAS, or when there is forward rotation of the ciliary body. These can occur after surgery or trauma, in idiopathic inflammatory conditions, or with specific uveitis entities such as interstitial keratitis,271 sarcoidosis,272 ankylosing spondylitis,273,274 pars planitis,275 and juvenile rheumatoid arthritis, particularly the pauciarticular variety.276–279 Peripheral anterior synechiae form more readily in eyes with shallow anterior chambers and in eyes afflicted with chronic granulomatous inflammatory disease.
Secondary angle-closure glaucoma without pupillary block is usually managed with medical therapy. It is crucial that residual inflammation be suppressed with corticosteroids. However, the ophthalmologist must keep in mind the possibility of inducing corticosteroid glaucoma. Patients are often more comfortable
222
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chapter |
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Secondary angle-closure glaucoma |
16 |
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Table 16-1 Differential diagnosis of the postoperative flat anterior chamber |
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Malignant Glaucoma |
Choroidal |
Pupillary Block |
Suprachoroidal |
Wound Leak |
|
|
|
Detachment |
|
Hemorrhage |
|
|
|
|
|
|
|
|
|
Central anterior |
Flat or shallow |
Shallow |
May be normal |
Flat or shallow |
Flat or shallow |
|
chamber |
|
|
|
|
|
|
|
|
|
|
|
|
|
Intraocular pressure |
Normal or elevated |
Low |
Normal or elevated |
Normal or elevated |
Low |
|
|
|
|
|
|
|
|
Fundus appearance |
Usually normal |
Large, smooth, |
Usually normal |
Dark brown or dark |
Choroidals may be |
|
|
|
brown mass |
|
red elevation |
present |
|
|
|
|
|
|
|
|
Suprachoroidal fluid |
Absent |
Present |
Absent |
Present |
Absent |
|
|
|
|
|
|
|
|
Relief by drainage of |
No |
Yes |
No |
Yes |
No |
|
suprachoroidal fluid |
|
|
|
|
|
|
|
|
|
|
|
|
|
Relief by iridectomy |
No |
No |
Yes |
No |
No |
|
|
|
|
|
|
|
|
Patent iridectomy |
Yes |
Yes |
No |
Yes |
Yes |
|
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|
|
|
Onset |
Usually within days, |
Usually within |
Anytime |
Immediately or within |
Usually within first few |
|
|
but may be months |
first week |
|
first few days |
days but may be late with |
|
|
|
|
|
|
adjunctive antimetabolites |
|
|
|
|
|
|
|
|
Seidel test |
Negative |
Negative |
Negative |
Negative |
Positive |
|
Modified from Simmons RJ, Maestre FA: Malignant glaucoma. In: Ritch R, Shields MB, Krupin T, editors: The glaucomas, 2nd edn, St Louis, Mosby, 1996.266
Fig. 16–9 Histopathology of anterior synechia formation following postoperative flat anterior chamber.
(Courtesy of William H Spencer, MD.)
with the addition of cycloplegic agents which may, by dilating the pupil, prevent pupillary block from posterior synechiae formation. Virtually all topical glaucoma agents are used to control IOP, with two guarded exceptions. Miotics may be helpful in the pseudophakic eye if it is quiet, but they are usually counterproductive in the presence of persistent inflammation. Similarly, prostaglandins should be used with caution because they may occasionally precipitate an inflammatory reaction.280 Hyperosmotic agents are administered on occasion for acute elevations of IOP.
If medical therapy fails to control IOP, filtering surgery must be considered. Because standard filtering surgery is less likely to be successful in inflamed eyes (and these patients are often young people), filtering surgery with adjunctive antimetabolite therapy or glaucoma drainage devices such as the Molteno, Baerveldt, or Ahmed implants should be performed. In children with inflammatory
disease the prospects for successful filtering surgery are further reduced by rapid healing, low scleral rigidity, and the increased thickness of Tenon’s capsule.281 A few authorities have used a modified goniotomy procedure – trabeculodialysis – to treat children with inflammation and glaucoma. A goniotomy knife is used to depress the iris and lyse any PAS present.The trabecular meshwork is then incised below Schwalbe’s line, and the trabecular tissues are retracted further.282,283
Penetrating keratoplasty
Angle-closure glaucoma can develop after penetrating keratoplasty, from mechanisms including pupillary block, postoperative inflammation, or a flat anterior chamber from a wound leak. The severity of the glaucoma is generally related to the extent of the synechial closure. The incidence of postkeratoplasty angle closure is reduced by performing one or more iridectomies, closing the wound meticulously, using a graft slightly larger than the recipient bed, and administering corticosteroids postoperatively.284–286 However, in some cases the iris becomes attached to the corneal wound, and it is pulled forward in progressive fashion. Glaucoma of one sort or another is a complication in about 20% of penetrating keratoplasties.287
Most cases of postkeratoplasty angle-closure glaucoma without pupillary block can be managed with standard medical treatment. Many of these eyes are aphakic and respond well to cholinesterase inhibitors, -blockers, -adrenergic agonists, prostaglandins, and carbonic anhydrase inhibitors. If pupillary block is contributing to the glaucoma, a laser iridotomy should be performed. Laser trabeculoplasty may be helpful, provided that at least one-third to onehalf of the angle is open.288 When medical treatment fails to control the glaucoma, filtering surgery with mitomycin-C can be successful if conjunctiva is not heavily scarred.289 However, the surgeon must proceed with care to avoid damage to the corneal graft. Filtering surgery alone often fails.290 A posterior glaucoma drainage device
223
