- •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
7 Laser Therapy
by having the patient gaze upwards, especially while enlarging the perforation.When the laser energy strikes the iris, a deep pit is produced.These signs indicate that the iris is relatively soft and absorbs the laser energy well so that iridotomy will be easily accomplished.
Initial power settings should be 600–1000 mW with a spot size of 50 m and a shutter speed of 0.02–0.05 second. Repeated applications of the laser in the center of the pit produced by the first shot will result in a 200to 300- m crater in the iris stroma. When the pigment epithelium is penetrated, a cloud of pigment will come out of the pit. Shutter speed can then be reduced to 0.02 second to remove the pigment epithelium from the depths of the pit and create an opening that is at least 0.2 mm in diameter. This is best done by chipping away at the edges of the small initial opening in the pigment epithelium by aiming the laser beam so that two-thirds of the beam is on the pigment epithelium and onethird is in the opening. Again, the surgeon should avoid aiming the laser toward the posterior pole by asking the patient to look up.
This technique usually produces a complete iridotomy with 10–20 shots in a light brown iris.
Dark brown iris
The densely pigmented dark brown iris has a uniform surface with no apparent thin areas. Charring of the surface occurs frequently with exposure times of longer than 0.05 second.This char appears as black shiny material (‘carbon’) at the laser application site. Additional laser applications do not penetrate the char, and instead of forming a coherent single bubble, multiple tiny bubbles spray off the surface after each application. After such charring occurs, it is very difficult, if not impossible, to penetrate that area, and a new location must be chosen. Another option is to use the Nd:YAG laser to perforate the charred site.
To avoid charring, short exposure times of 0.02–0.05 second should be used with initial power settings of 400–1000 mW and a spot size of 50 m. If a reasonable pit develops in the iris, these settings can be continued, striking the same spot and slowly advancing the focal point until perforation of the pigment epithelium is recognized by formation of the typical pigment cloud.The hole is then enlarged in the same manner as with light brown irides.
If a pit does not develop or is very small, power can be increased in 200-mW increments until an effective power is obtained. It is rarely necessary to go above 1000 mW. Exposure times should not be increased above 0.10 second because charring is very likely with longer exposures. Completion of an iridotomy can usually be accomplished with 20–50 applications.
Light blue iris
Blue or pale grey irides have insufficient stromal pigment to absorb laser energy.The energy can pass directly through the stroma, leaving it intact, and separate the pigment epithelium from the back of the iris. This can be recognized as a transillumination defect in the iris with intact overlying stroma. Subsequent shots simply pass through the iris stroma without creating a hole (Fig. 30-6).
Occasionally a small pigmented area, which will respond much like a light brown iris, may be found in an appropriate site for iridotomy. If there is no pigmented area, longer exposures will generate heat in the pigment epithelium; the heat is then transmitted into the stroma and destroys it. The surgeon’s goal is to create a bubble at the laser site before the pigment epithelium is destroyed. Then, by firing additional shots through the apex of the bubble, the stroma is destroyed, exposing the underlying pigment epithelium.41
The initial setting should be a 200- m spot, 200–400 mW, 0.1 second duration to anneal the pigment epithelium to the stroma.
Fig. 30-6 Argon laser peripheral iridotomy in a light blue iris. The argon beam may pass directly through the light blue stroma and blast the pigment off the back of the iris. Subsequent laser applications will pass through the stroma without affecting it because there is no adjacent pigmented material to absorb the energy.
Then the spot size is reduced to 50 m and the power increased to 600–1000 mW at 0.02–0.1 second to perforate. If the stroma is clearly being treated, as evidenced by its clumping and opacification, then these settings can be continued. If penetration has not occurred in 20–40 shots, then a new spot should be treated with an alternative technique.
One alternative technique requires higher energy (1200– 1500 mW), with exposure times of 0.3–0.4 second and a 50- m spot size.The shutter speed is set at 0.5 second. As the firing pedal is depressed, a bubble will form.When the bubble is about 0.5 mm in diameter, the pedal is released. Before the bubble can float away, a second laser application is fired directly through the apex of the bubble (Fig. 30-7). Occasionally a third such application is required. These initial high-energy shots will create a crater whose base is the pigment epithelium. It is then a simple matter to remove the pigment epithelium by using shorter exposures (0.05–0.1 second) at lower energies (400–600 mW), as described for brown irides.
Another alternative uses low-energy ‘stretch’ burns of 200 mW and a 200- m spot size for 0.1–0.2 second on either side of (or surrounding) the site to be perforated. The concept behind this technique is to tighten the iris between the stretch burns, making iris perforation easier. Most iridectomies can be performed without this additional trauma.
Complications of laser iridotomy
Iritis
Some degree of iritis always follows laser iridotomy. Iritis can be minimized by topical corticosteroid eyedrops (e.g., prednisolone acetate 1% hourly until bed time on the day of laser treatment and four times daily for the following day or two), but most patients do quite well without treatment. Sometimes, following argon or diode laser iridotomy, posterior synechiae develop. Occasionally patients develop recurrent iritis after laser iridotomy.This represents aggravation of a pre-existing condition in most patients but rarely arises de novo after the laser therapy. Hypopyon is rare.
Pressure elevation
Preventive therapy to limit a potential rise in IOP is recommended. Intraocular pressure elevation commonly occurs 1–4 hours after laser iridotomy and is usually self-limited. Elevations greater than 10 mmHg are seen in roughly 17–27% of patients.42,43 Treatment
442
|
chapter |
Laser treatment for internal flow block |
30 |
|
|
Iris
(A) |
(B) |
Fig. 30-7 (A) Bubbles are often created at the site of laser impact into the iris tissue and can be advantageous, transferring greater energy from each application into the iridotomy site. (B) A bubble captured in the iris stroma acts much like a concave mirror redirecting reflected energy back into the iris stroma. Where the iris pigment epithelium is in contact with the stroma, the laser energy escapes from the bubble and is absorbed by the tissue. The bubble enhances the effect of the laser energy, allowing development of a crater in the iris surface with fewer applications. However, if the bubble is in contact with the corneal endothelium, the laser energy will be absorbed by the endothelium and cause an endothelial burn.
options include the use of an -adrenergic agonist (Iopidine 0.5–1%,42 Alphagan 0.2%), a -blocker (Timoptic 0.5%, Betoptic 0.5%), carbonic anhydrase inhibitors (Trusopt 2%, Diamox, Neptazane), or an osmotic agent (Ismotic). Most recommend either topical apraclonidine or topical brimonidine, one drop before treatment, and some add one drop after.
Usually the IOP returns to pretreatment or lower levels within 24 hours. In combined-mechanism forms of glaucoma in which the outflow is abnormal before laser therapy, however, the IOP elevation can be severe and sustained. Such patients should be warned before undergoing laser surgery that filtering surgery may be required to control this pressure elevation. This complication is more likely if high IOP is associated preoperatively with a chamber angle that, although quite narrow, is open, so that aqueous has access to the trabecular meshwork. These findings indicate that although the incomplete angle closure may be contributing in part to the IOP elevation, the trabecular meshwork is not functioning adequately.The trauma of the laser iridotomy and the pigment released may further tax the meshwork, precipitating the need for filtering surgery.
Cataract
Cataract formation can occur after surgical iridotomy. Follow-up of patients who had argon laser iridotomies indicates that the laser
treatment has no greater likelihood of causing cataract than does surgical iridectomy.26,44–48
Argon laser iridotomy frequently causes localized injury to the lens beneath the iridotomy site. The injury can be seen as a whitening of this area of the lens. Fortunately, long-term follow-up has shown that these focal opacities do not progress. Nd:YAG iridotomy has caused lens capsule perforation in monkeys.49 Obviously the Nd:YAG laser can rupture the capsule in humans as well, thus focus is critical.This complication is rare.
It is reasonable to assume that iridotomy (surgical or laser) is a traumatic experience to the eye. Mild postoperative iritis is common and may be responsible for the metabolic lens changes that accelerate cataract formation.
In some patients undergoing extracapsular cataract surgery, zonular weakness in the area of the argon laser iridotomy has been noted. It is conceivable that the laser peripheral iridotomy may have damaged these zonules.
Hyphema
Hyphema is a rare occurrence with argon laser iridotomy50 but is common after Nd:YAG laser iridotomy. The bleeding is usually self-limited and of little consequence except that it may contribute to transient IOP elevation and reduced vision.51 Temporary IOP elevation created by pressing on the contact lens is usually adequate to control the bleeding site.
Corneal epithelial injury
Corneal epithelial injury occurs commonly with laser iridotomy. If high energy levels are used, if a chromophore such as fluorescein is on the corneal surface, or if the epithelium is slightly edematous, small white burns may appear. All evidence of any topical dye should be gone before attempting laser iridotomy with argon or diode lasers.When burns do occur, they disappear after a day or so without long-term effects. Use of a contact lens helps minimize corneal burns in most patients.
Endothelial damage
Endothelial damage also occurs with argon, solid-state, and Nd: YAG laser iridotomy (Fig. 30-8).52–54 If the iris is very near or
touching the cornea, both types of laser can cause burns. If a bubble is pressed against the endothelium at the point of laser impact or if the laser is focused poorly, an endothelial burn will occur with photothermal laser energy.
Epithelial and endothelial burns reduce both corneal clarity and the amount of laser energy reaching the iris, making the procedure more difficult. If burns occur, power or exposure time should be reduced. If it is not possible to avoid the burn by changing the approach, a new site should be chosen. Extensive endothelial burns can lead to persistent corneal edema. Nd:YAG laser treatments close to the endothelium can also cause tiny glass-like cracks at Descemet’s membrane.
443
