- •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
|
chapter |
Miscellaneous laser procedures including laser ciliary body therapy |
32 |
|
|
times range from 10 to 20 ms. Some surgeons use up to 8 J. Because of the varying amounts of energy delivered by each type of laser instrument, it is advisable to obtain recommendations from a surgeon experienced with the particular instrument being used.
Although repeat treatments often are needed, 60–70% of cases can be controlled, maintaining IOPs of 22 mmHg or lower. Complications include reduced visual acuity, uveitis, pain, hemorrhage, and phthisis bulbi. All of these complications, especially pain and inflammation, seem less severe than those experienced after cyclocryotherapy.
Contact trans-scleral cyclophotocoagulation (TCP) (Fig. 32-3) has been accomplished using the same laser energy levels but deliv-
ered with a fiber-optic probe lightly pressed onto the conjunctiva (Tables 32-1 and 32-2).14–17 Slightly lower energy levels than those
Fig. 32-3 Superior conjunctiva immediately after contact TCP. Small depressions in the conjunctiva disappear within minutes and the eye often appears essentially normal in 24 hours.
Table 32-1 Trans-scleral contact cyclophotocoagulation techniques
|
1064-nm Nd:YAG |
810-nm Diode |
|
|
|
Power |
5–6 J14 |
1.5–2.5 W, 1–2 sec15 |
Lesions |
30–40 |
16–18 |
Distance from limbus |
0.5–1 mm |
1.2 mm |
Spot size |
0.9 mm |
100–400 m |
used for non-contact procedures are advisable because the contact pressure increases the transparency of the sclera. Retrobulbar anesthesia is necessary, as is a speculum to separate the eyelids.The probe should be placed 0.5–1.0 mm from the limbus and held as perpendicular to the sclera as possible. Probes made especially for cyclophotocoagulation such as the G-Probe™ of Gaasterland make placement easier and more uniform.18
All forms of trans-scleral laser cyclophotocoagulation may damage ciliary muscle as well as ciliary epithelium, adjacent iris, and retina. Extreme care must also be taken to avoid excessive destruction of the ciliary body, which could lead to hypotony and possibly phthisis.To target the ciliary epithelium more accurately, some physicians favor the use of an endoscopic probe and laser delivery fiber introduced via a limbal incision.19 This allows the surgeon to directly visualize and destroy the ciliary processes.20 This is an invasive technique, however, that requires sterile technique but is gaining in popularity.
Endocyclophotocoagulation procedures are currently under clinical and laboratory investigation. Endocyclophotocoagulation may be most useful for aphakic and pseudophakic eyes or in combination with phacoemulsification procedures.21,22 Following endocyclophotocoagulation, some surgeons inject sub-Tenon’s dexamethasone over the perilimbal area treated by the laser; others use topical steroids and atropine drops alone.
Since immediate postoperative pressure spikes are common with all types of cyclophotocoagulation, often an oral carbonic anhydrase inhibitor (acetazolamide 500 mg, methazolamide 50– 100 mg) is administered immediately preor postoperatively. It is important to monitor patients closely in the short-term postoperative period.
The operated eye is usually patched postoperatively overnight or until the anesthetic wears off. Long-acting anesthetics such as bupivacaine help with immediate postoperative pain control. The patient should be sent home with an adequate supply of major analgesic medication as the eye may be quite painful after the anesthetic wears off. Topical regimens typically include prednisolone acetate 1% four times daily and atropine sulfate 1% twice daily. Medications are tapered gradually until inflammation has disappeared. Preoperative glaucoma medications may be continued as needed, except for miotics. Repeat cyclodestructive procedures are often necessary, although fewer spots should be treated to avoid hypotony and phthisis.
These procedures are alternatives to cyclocryotherapy. All cyclodestructive procedures may cause side effects of pain, phthisis, and reduced vision, although laser techniques may cause less pain and allow for more precise control of energy delivery.
Table 32-2 Trans-scleral non-contact cyclophotocoagulation techniques
|
1064-nm Nd:YAG |
810-nm Diode |
|
|
|
Power |
4–8 J16 |
1200–1500 mW, 1 sec17 |
Lesions |
30–40 |
30–40 |
Distance from limbus |
1–2 mm |
0.5–1.0 mm |
Spot size |
0.9 mm |
100–400 m |
Depth of focus |
3.6 mm beyond surface |
3.6 mm beyond surface |
Other laser procedures
Lasers have also achieved widespread use in conjunction with surgical procedures such as trabeculectomy. Laser suture lysis, for example, can safely sever trabeculectomy flap sutures to increase filtration. Laser bleb reopening and remodeling may reduce the need for further invasive filtration surgery. Finally, lasers provide a safe and often effective approach to closing cyclodialysis clefts, removing peripheral anterior synechiae from the angle or cornea, and enlarging miotic pupils. Laser procedures are safer than surgical alternatives in all of these capacities.
457
part
7 laser therapy
Severing of sutures
Subconjunctival trabeculectomy flap sutures can be lysed with the laser postoperatively if there is inadequate filtration. Dark nylon or proline sutures can usually be severed with the argon laser using settings of 200–1000 mW for 0.02–0.15 second with a 50–100- m spot size.23 This allows the surgeon to suture the wound more securely at the time of surgery.24,25 Tighter suturing maintains the integrity of the eye better and reduces the incidence of flat chambers and hypotony in the early postoperative period. The procedure is feasible from about 3–15 days after surgery or up to at least 2 months or more after mitomycin-C use.26
Laser suture lysis (LSL) is accomplished by first anesthetizing the eye with an appropriate topical agent and then compressing the conjunctiva overlying the suture with the flat corner of a fourmirror gonioprism or specially designed laser suture lens such as that described by Hoskins.23 Phenylephrine 2.5% or apraclonidine 0.5% (Iopidine®) is useful to blanch the superficial vessels of the conjunctiva. Gentle but constant pressure with the lens will displace fluid from the most edematous conjunctiva and provide a clear view of the underlying suture, which usually can be lysed with one or two laser applications. If possible, sutures should be lysed close to their tissue penetration site to prevent the loose ends from springing up and potentially disrupting the conjunctiva.Very edematous flaps may require 1–2 minutes of sustained gentle pressure over the suture before the suture is clearly visible (Figs 32-4 and 32-5). Dense hemorrhage in the tissues overlying the suture will absorb the energy, prevent treatment, and possibly cause conjunctival perforation. Similarly, fluorescein-stained conjunctiva limits argon laser energy transmission to the sutures and may cause conjunctival perforation. Therefore eyes with conjunctival hemorrhage obscuring the suture cannot be treated with this technique.
A thick, inflamed Tenon’s capsule may also preclude successful LSL.This is unfortunate because these eyes commonly suffer from inadequate filtration. After the suture is cut, gentle pressure on the scleral edge of the incision will elevate the bleb and increase flow.
Fig. 32-4 Laser suture lens. The device has a small convex lens that compresses the edematous conjunctiva, permitting a clear view of the tiny nylon suture underneath the conjunctiva. This suture then can be cut easily with a 50- m spot laser beam using 400 mW of energy for 0.1 second.
(Photo courtesy of John Hetherington Jr, MD, University of California, San Francisco.)
Topical steroids are often useful postoperatively to reduce external scarring. An important point to remember is that only one suture should be severed at a time because excessive filtration might occur,23 leading to a flat anterior chamber. The eye should be examined carefully after the LSL session to ensure that the wound is intact. Additional sutures can be lysed 1 or 2 days later if filtration is still inadequate.
Reopening failed filtration sites
Filtering sites can close because of fibrosis on the external side beneath the conjunctiva or because of membrane formation or iris incarceration on the internal side of the sclerostomy. In any case, if the bleb is to be salvaged, reopening should be attempted early, before the episclera has completely closed the external opening at the sclerostomy because of lack of aqueous flow.
A Goldmann three-mirror goniolens or specially designed laser goniolens is used to view the internal site. If pigmented tissue is
obstructing the sclerostomy, the argon or Q-switched Nd:YAG laser can vaporize it.27–29 With the argon laser, settings of 300–
1000 mW at 0.1–0.2 second with a 50–100- m spot are used. If the obstruction is a pillar of iris, the laser is directed toward one side of the anterior edge of the iridocorneal adhesion. If the attachment is
(A)
(B)
Fig. 32-5 (A) When lasering sutures, the flange of the Hoskins laser suture lens holds up the lid. The suture is located under the laser slit lamp. (B) The lens is pressed steadily against the conjunctiva, displacing edema until a clear image of the suture is seen (upper right). The suture usually is treated near the knot. The long end of the suture will then retract into the sclera (lower right).
458
|
|
|
|
|
chapter |
|
Miscellaneous laser procedures including laser ciliary body therapy |
32 |
|||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
(A) |
Fig. 32-7 Closure of a cyclodialysis cleft. The beam is aimed deep into |
|
|
|
the cleft to create an inflammatory response and generate closure. |
|
|
Postoperative mydriasis and cycloplegia may aid this process. |
|
|
|
(B)
Fig. 32-6 (A) Before Nd:YAG laser therapy. Despite what appeared to be a healthy bleb, the pressure was 30 mmHg in this eye. Note the dense white membrane existing beneath the bleb surface. (B) After Nd:YAG laser therapy. The Nd:YAG laser was focused deep into the bleb with four applications at 8 mJ. Note the dark area where the whitish membrane had been. Intraocular pressure fell immediately to 18 mmHg, and the bleb enlarged.
not too solid, the synechiae can be dissected away from the sclerostomy site with similar settings on the argon laser by freeing up one edge of the synechia with laser applications and gradually working across the line of iridocorneal adhesion with additional laser applications. Pigmented tissue within the site should also be vaporized.
The Nd:YAG laser is also useful in opening an obstructed sclero- stomy.5,30–33 Single bursts of 2–4 mJ are delivered via a Nd:YAG-
coated goniolens to disrupt any translucent membrane obstructing it. Lower power levels (i.e., 1–2 mJ) should be used initially to dissect any iris adhesions. Bleeding may obscure the view, requiring a delay between treatments, but this is rarely serious.
Laser treatment may produce an instantaneous lowering of IOP, or approximately 1 day may be required for the pressure to fall. Digital pressure applied three to four times daily may be helpful. An increase in the size of the bleb indicates that the sclerostomy has indeed been opened and that the pressure decline is not simply a result of inflammation.
Blockage occurring on the episcleral side of the bleb rarely can be opened.The Nd:YAG laser can be used through translucent tis-
sue to rupture pigmented or non-pigmented membranes overlying sclerostomy sites.34,35 It is essential that the laser be focused at least
0.5 mm internal to the surface of the bleb or else the shock wave, which expands toward the surgeon from the point of focus, will rupture the overlying bleb (Fig. 32-6). This is especially true with thin blebs such as those seen after mitomycin-C use.
In all of these situations it is advisable to start with a lower power level, increasing it as indicated by the tissue reaction. Success with
any of these procedures is limited, but their simplicity encourages an attempt.
Cyclodialysis and laser
Cyclodialysis clefts have been both opened and closed with laser.36 Most reports are limited to a relatively small number of cases because cyclodialysis is rarely seen.37–39 A variety of successful techniques have been employed.40,41 One patient undergoing a cyclodialysis in conjunction with trabeculectomy had the cyclodialysis reopened 2 months after filtering surgery. A hyaline membrane covering the cleft was divided with a Q-switched Nd: YAG laser using a single pulse of 3.8 mJ. Postoperative treatment included strong miotics and corticosteroids.42
Argon laser photocoagulation using thermal burns of 0.1 second, 100- m spot size, and 500 mW can be used to close cyclodialysis clefts and reduce hypotony (Fig. 32-7).Three patients have reportedly had successful long-term effects.43 In these patients, up to 100 burns were delivered to the area in and around the clefts posterior to the scleral spur.43 Postoperative treatment should include topical steroids and cycloplegics.
Sudden rises of IOP often occur after closure of cyclodialysis clefts.These usually require aqueous suppression therapy.43
Laser synechialysis
The argon laser can be used to pull early or lightly adherent peripheral anterior synechiae away from the angle or cornea. Settings similar to those used for iridoplasty (400–800 mW, 0.1–0.2 second, 50–100- m spot size) are used. If used early, this may be helpful to break and arrest formation of iridocorneal adhesions after penetrating keratoplasty or other forms of peripheral anterior synechiae.This procedure is most likely to work if it is performed very soon after the synechiae have formed. Chronic synechiae can be very resistant to argon iridoplasty. If it is obvious after the first few applications that the iris is firmly adherent, it is useless to persist because this will only cause additional iritis.44
The Nd:YAG laser can lyse iris adhesion. This technique may be useful in early irido–corneal–endothelial (ICE) syndrome to disrupt synechiae, although bleeding may occur. This procedure is also used for reopening filtration blebs and sometimes for preventing further peripheral anterior synechiae after penetrating keratoplasty.45 Nd:YAG lysis of posterior synechiae has been used
459
