- •Pearls of Glaucoma Management
- •Optic Nerve: The Glaucomatous Optic Nerve
- •1.1 Why is the Optic Nerve Important in the Diagnosis and Management of Glaucoma?
- •1.1.1 The Optic Nerve Head (ONH) is the Principal Site of Glaucomatous Damage to the Visual System
- •1.1.3 The Clinical Appearance and Behavior of the ONH Holds Clues as to the Etiology of a Given Optic Neuropathy
- •Summary for the Clinician
- •References
- •Optic Nerve: Clinical Examination
- •Summary for the Clinician
- •2.2 How Does One Establish the Borders of the Nerve and Follow the Neuroretinal Rim Contour?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •2.6 How Quickly Can I Expect Optic Nerve Change to Occur?
- •Summary for the Clinician
- •2.7 If I See a Disc Hemorrhage on Healthy Appearing Neuroretinal Rim, How Soon Can I Expect to See a Change in the Rim?
- •Summary for the Clinician
- •References
- •Optic Nerve: Heidelberg Retinal Tomography
- •3.1 What Indices Should I Use to Help Me Interpret the Heidelberg Retinal Tomograph (HRT) Printout?
- •Summary for the Clinician
- •3.2 How Big a Change is Meaningful in the Numbers on an HRT Printout?
- •Summary for the Clinician
- •3.3.1 Trend Analysis
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Optic Nerve: Scanning Laser Polarimetry
- •4.1 What is the Physical Principle Behind Scanning Laser Polarimetry (SLP)?
- •4.1.1 How has Scanning Laser Polarimetry Evolved?
- •4.1.2 What is GDxVCC (Variable Corneal Compensation)?
- •4.1.3 What is GDxECC (Enhanced Corneal Compensation)?
- •Summary for the Clinician
- •4.2 How is Image Quality and Artifact Assessed on the GDxVCC Printout?
- •Summary for the Clinician
- •Summary for the Clinician
- •4.4.1 Detection of Progression with SLP
- •Summary for the Clinician
- •References
- •Optic Nerve: Optical Coherence Tomography
- •Summary for the Clinician
- •5.2 What Indices Should I Use to Help Me Interpret the “RNFL Thickness Average Analysis Report” Printout?
- •Summary for the Clinician
- •Summary for the Clinician
- •5.4 Can I Use OCT Clinically to Diagnose Glaucoma? How Certain Can I Be that the Diagnosis is Real?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Optic Nerve: Comparison of Technologies
- •6.1 Why Image the Optic Nerve?
- •6.1.3 Scanning Laser Polarimetry (SLP)
- •Summary for the clinician
- •Summary for the Clinician
- •6.3 Is One Imaging Technique Easier to Use and Interpret than Another?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •7.1 Should Peripapillary Atrophy (PPA) Concern Me? Should it Be Followed for Enlargement?
- •Summary for the Clinician
- •7.2 In Examining Tilted Optic Discs, How Do I Distinguish Tilt vs. Glaucoma?
- •7.2.1 What are the Characteristics of a Tilted Disc?
- •7.2.5 What Management Strategy Can I Use in Equivocal Cases of Tilt vs. Glaucoma?
- •Summary for Clinicians
- •7.3 With Optic Nerve Head Drusen (OND), How Do I Tell If Visual Field Changes are due to Drusen vs. Glaucoma?
- •7.3.1 Description of Drusen
- •7.3.2 What are the Characteristics of Field Defects in OND?
- •7.3.3 Are There Other Signs that Can Help Me Distinguish Between OND and Glaucoma?
- •7.3.4 Can Imaging Help Me to Distinguish Between OND and Glaucoma?
- •7.3.5 What Management Strategy Can I Use in Equivocal Cases of OND vs. Glaucoma?
- •Summary for the Clinician
- •7.4.1 What is the Significance of Disc Cupping?
- •7.4.3 What is the Significance of Optic Disc Pallor?
- •Summary for the Clinician
- •References
- •8.1 Why is Intraocular Pressure Important in Diagnosing and Treating Glaucoma?
- •8.1.3 Non-IOP Factors May also Be Involved in the Pathogenesis of Glaucoma
- •8.1.4 The Decision to Initiate Treatment by Lowering IOP
- •Summary for the Clinician
- •References
- •IOP: Instruments to Measure IOP
- •9.2.1 Maklakov Tonometer
- •9.2.2 Shiøtz Tonometry
- •9.2.3 Goldmann Tonometry
- •9.2.4 McKay-Marg and Tonopen
- •9.2.5 Air-Puff Tonometry
- •9.2.6 Dynamic Contour Tonometry
- •9.2.7 Trans-Palpebral Tonometers
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •9.5 In Cases of Prosthetic Corneas How Can I Measure the IOP?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •IOP: Central Corneal Thickness
- •10.1.1 Goldmann Tonometry
- •10.1.2 The Influence of CCT on Tonometry
- •Summary for the Clinician
- •10.2.1 CCT in Different Populations
- •10.2.2 CCT Over Time
- •Summary for the Clinician
- •10.3 Does CCT Predict Glaucoma?
- •10.3.1 Clinical Trials
- •10.3.2 CCT in Established Glaucoma
- •10.3.3 CCT as a Biological Risk Factor
- •Summary for the Clinician
- •10.4.1 Should IOP Be “Adjusted” for CCT?
- •10.4.4 Should I Measure CCT in All Patients?
- •Summary for the Clinician
- •References
- •IOP: Corneal Hysteresis
- •11.1 What is Corneal Hysteresis and How Does it Influence IOP Measurement?
- •Summary for the Clinician
- •Summary for the Clinician
- •11.3 What Is the Relationship Between CCT, IOP, and Corneal Hysteresis?
- •Summary for the Clinician
- •11.4 Should I Invest in Newer Devices to Measure IOP that Claim Less Influence of CCT?
- •Summary for the Clinician
- •References
- •IOP: Target Pressures
- •Summary for the Clinician
- •12.2 If I Decide to Set a Target IOP, How Should I Set it – Do I Use a Percent Reduction or Aim Toward an Absolute Number?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •IOP: Fluctuation
- •13.1 Why is IOP Fluctuation a Topic of Interest?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •13.5 What is the Significance of Measures of Long-Term IOP Fluctuation?
- •Summary for the Clinician
- •13.6 What is the Impact of Medication on Short-Term and Long-Term IOP Fluctuation?
- •Summary for the Clinician
- •13.7 What is the Impact of Surgery on Short-Term and Long-Term IOP Fluctuation?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Gonioscopy: Why Do Indentation?
- •14.1 Which Patients Should have Gonioscopy?
- •Summary for the Clinician
- •14.2 Of What Use is the Van Herick Angle Examination?
- •Summary for the Clinician
- •14.3 What Lens Should be Used for Gonioscopy?
- •Summary for the Clinician
- •Summary for the Clinician
- •14.5 What Should I Look for in the Angle?
- •Summary for the Clinician
- •14.7 How Narrow is too Narrow? What are the Indications for Laser Iridotomy in a Patient with No Symptoms of Angle-closure?
- •Summary for the Clinician
- •14.8 What Should I Know about Plateau Iris?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Visual Fields: Visual Field Test Strategies
- •15.1.1 Automated vs. Manual
- •Summary for the Clinician
- •Summary for the Clinician
- •15.3 Is There a Visual Field Program of Choice at This Point in Time?
- •Summary for the Clinician
- •Summary for the Clinician
- •15.5 What Program is Best for Use in a General Clinic to Screen for Glaucoma?
- •Summary for the Clinician
- •15.6 How Can I Convert from One Visual Field Strategy to Another to Help Me Interpret and Compare Tests?
- •Summary for the Clinician
- •15.7 What Can be Done to Obtain Visual Field Information in a Patient who Consistently Tests Unreliably?
- •Summary for the Clinician
- •References
- •Visual Fields: Fluctuation and Progression
- •16.1 How Do I Distinguish Between Fluctuation and True Progressive Change on Visual Field Printouts?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •16.4 What Automated Progression Analysis Software Is Available to Help with Visual Field Interpretation?
- •Summary for the Clinician
- •References
- •Visual Fields: Field Interpretation
- •17.1 How Is Information on a Single Field Printout of the Humphrey Visual Field Analyzer Interpreted?
- •17.1.1 Part 1 of the Visual Field Printout
- •17.1.2 Part 2 of the Visual Field Printout
- •17.1.3 Part 3 of the Visual Field Printout
- •17.1.4 Part 4 of the Visual Field Printout
- •Summary for the Clinician
- •17.2 How Is the Information on the Glaucoma Progression Analysis Printout Interpreted?
- •17.2.1 Part 1 of the GPA Printout
- •17.2.2 Part 2 of the GPA Printout
- •17.2.3 Part 3 of the GPA Printout
- •Summary for the Clinician
- •17.3.2 Automatic Reliance on the Statistical Analysis
- •17.3.3 Visual Field Artifacts
- •Summary for the Clinician
- •References
- •Other Tests in Glaucoma: Genetic Testing
- •18.1.1 Anterior Segment Dysgenesis
- •18.1.3 Congenital Glaucoma
- •18.1.4 Low-Tension Glaucoma
- •18.1.6 Pseudoexfoliation Glaucoma
- •Summary for the Clinician
- •18.2 Are Genetic Tests for Glaucoma of Practical Use in a Clinical Setting Today, or Are They More of Theoretical Use?
- •18.2.1 Anterior Segment Dysgenesis
- •18.2.3 Congenital Glaucoma
- •18.2.4 Low-Tension Glaucoma
- •Summary for the Clinician
- •18.3 How Do I Collect Samples and Where Do I Send Them for Analysis?
- •Summary for the Clinician
- •18.4.1 Genetic Counseling
- •18.4.3 Juvenile-Open Angle Glaucoma
- •18.4.4 Congenital Glaucoma
- •18.4.5 Low-Tension Glaucoma
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •19.2 Is Abnormal Ocular Blood Flow Causal in Glaucoma and Glaucoma Progression, and Does It Correlate with Disease Severity?
- •Summary for the Clinician
- •19.3.1.2 Patients with Vasospasm
- •19.3.1.3 Patients with Nocturnal Blood Pressure Dips
- •19.3.1.4 Diabetes
- •19.3.2 Patients Who Progress despite Reaching Target IOP or with Fluctuating IOP and Pulse Pressure
- •19.3.3 NTG Patients with Migraine and or Disc Hemorrhages
- •Summary for the Clinician
- •19.4 What are the Most Common Techniques to Measure Optic Nerve Blood Flow and what are Their Limitations?
- •19.4.1 Color Doppler Imaging (CDI)
- •19.4.4 Angiography
- •Summary for the Clinician
- •References
- •20.1 What Evidence Is There that Vascular Alterations Play a Role in Open-Angle Glaucoma (OAG)?
- •Summary for the Clinician
- •Summary for the Clinician
- •20.3.1 Color Doppler Imaging (CDI)
- •20.3.4 Laser Doppler Flowmetry (LDF)
- •20.3.5 Retinal Vessel Analyzer (RVA)
- •Summary for the Clinician
- •20.4.1 Color Doppler Imaging
- •20.4.2 Heidelberg Retinal Flowmeter
- •20.4.4 Laser Doppler Flowmetry
- •20.4.5 Retinal Vessel Analyzer
- •Summary for the Clinician
- •20.5.1 Color Doppler Imaging
- •20.5.2 Heidelberg Retinal Flowmeter
- •20.5.3 Canon Laser Blood Flowmetry
- •20.5.4 Laser Doppler Flowmetry
- •20.5.5 Retinal Vessel Analyzer
- •Summary for the Clinician:
- •20.6 How Can the Data from Ocular Hemodynamic Studies Be Used in Clinical Practice?
- •Summary for the Clinician
- •References
- •21.1.1 The Visual Evoked Potential (VEP)
- •Summary for the Clinician
- •Summary for the Clinician
- •21.3 Is the mfVEP a Useful Test in Glaucoma?
- •21.3.1 The mfVEP Is Not Ready for Routine Screening of Glaucoma Patients
- •21.3.2 The mfVEP Can Provide Clinically Useful Information
- •21.3.2.2 Unreliable Visual Fields
- •21.3.2.3 Inconsistent Visual Fields
- •21.3.2.3 Visual Fields that Need Confirmation
- •Summary for the Clinician
- •References
- •Risk Factors
- •Summary for the Clinician
- •22.2 What are the Main Risk Factors for Primary Open-Angle Glaucoma?
- •22.2.2 Demographic Factors
- •22.2.4 Central Corneal Thickness
- •22.2.5 Systemic Factors
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Risk Factors: The Risk Calculator
- •23.1 Is a Risk Calculator Useful?
- •Summary for the Clinician
- •23.2 How Should I Use a Risk Calculator?
- •Summary for the Clinician
- •23.3 Can I Screen for Glaucoma with a Risk Calculator?
- •Summary for the Clinician
- •23.4 What Does It Mean to Me and My Patient If the Risk Score Is High?
- •Summary for the Clinician
- •References
- •24.1 Should Beta Blockers Still Be Used as a First-Line Agent?
- •24.1.1 What is the Topical Beta Blocker Mechanism of Action?
- •24.1.2 What Magnitude of IOP Decrease Is Seen with Beta Blockers?
- •24.1.3 How Should Beta Blockers Be Initiated?
- •24.1.4 What Are the Differences Between Individual Beta Blockers?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •24.4 Should Miotics Still Be Used?
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •25.2 What Medications Are Safe to Use in a Nursing Mother?
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •26.2 How Should Oral CAIs Be Dosed?
- •Summary for the Clinician
- •Summary for the Clinician
- •26.4 Can CAIs Be Used in Pregnant Women or Pediatric Patients?
- •Summary for the Clinician
- •26.5 Can CAIs Be Used in Patients with Sickle Cell Anemia?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Medical Treatment: Osmotic Agents
- •27.1 When Using Hyperosmotics Agents, What Is a Typical Dose for Acutely Elevated Intraocular Pressure (IOP)?
- •Summary for the Clinician
- •Summary for the Clinician
- •27.3 Should Hyperosmotic Agents Be Used to Lower IOP Prior to Surgery?
- •Summary for the Clinician
- •References
- •Medical Treatment: Neuroprotection
- •28.1 What Exactly Is Neuroprotection?
- •Summary for the Clinician
- •Summary for the Clinician
- •28.3.1 Memantine
- •28.3.2 Brimonidine
- •28.3.3 Betaxolol
- •28.3.4 Calcium Channel Blockers
- •23.3.5 Other Possible Treatments
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •29.2 What Is the Natural History of Treated and Untreated Glaucoma?
- •29.2.1 Olmsted County, MN
- •29.2.2 St. Lucia Study
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •30.1.1 What Is Adherence?
- •30.1.2 What Is Persistence?
- •Summary for the Clinician
- •30.2 How Can One Help Patients to Be More Compliant with Treatment?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •31.2.1 Exercise
- •31.2.2 Smoking
- •31.2.3 Alcohol Consumption
- •31.2.4 Diet
- •Summary for the Clinician
- •31.3.1 Marijuana Use
- •31.3.2 Gingko Biloba
- •31.3.3 Bilberry
- •31.3.4 Acupunture
- •Summary for the Clinician
- •References
- •32.1.2 Does Trabeculoplasty benefit Compliance?
- •32.1.3 How well does Trabeculoplasty control the Diurnal IOP curve?
- •32.1.4 What are the Side Effects/Risks of Trabeculoplasty?
- •32.1.5 What are the Economic Issues Involved with Trabeculoplasty?
- •Summary for the Clinician
- •32.2.1 What is the Efficacy of ALT Versus SLT?
- •32.2.2 What are the Complications of ALT Versus SLT?
- •32.2.3 How does Retreatment compare between ALT and SLT?
- •Summary for the Clinician
- •32.3 When Should SLT or ALT not Be Performed?
- •32.3.1 Types of Glaucoma
- •32.3.2 IOP Reduction
- •32.3.3 Maximal Medical Therapy
- •Summary for the Clinician
- •32.4.1 Argon Laser Trabeculoplasty
- •32.4.2 Selective Laser Trabeculoplasty
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •32.7 What is the Mechanism of Action of ALT and SLT?
- •32.7.1 Mechanical Theory
- •32.7.2 Biologic Theory
- •32.7.3 Repopulation Theory
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •33.1 When Can or Should Endoscopic Cyclophotocoagulation (ECP) Be Used?
- •Summary for the Clinician
- •33.2 Should ECP Be Used as a Primary Surgery for Glaucoma?
- •Summary for the Clinician
- •33.3 Is Burning the Ciliary Processes a Safe Thing to Do?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •33.6 What Are Complications that May Be Encountered and How Are They Specifically Managed?
- •Summary for the Clinician
- •Summary for the Clinician
- •33.8 What Is the Long Term Safety Data on this Procedure?
- •Summary for the Clinician
- •References
- •34.1 What is Transscleral Cyclophotocoagulation (TCP)?
- •Summary for the Clinician
- •34.2 When Should I Use TCP? Should it be Used as a Primary Surgery for Glaucoma?
- •Summary for the Clinician
- •34.3 Technically, How is TCP Performed?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Procedural Treatments: Trabeculectomy
- •Summary for the Clinician
- •35.2 Should Antimetabolites be Used in All Cases of Trabeculectomy?
- •35.3 Do You Adjust Antimetabolite Usage and Dose Based on Patient Age or Race?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Procedural Treatments: Bleb Needling
- •37.1.1 Slit Lamp Bleb Needling
- •37.1.3 Antimetabolite Use with Needling
- •Summary for the Clinician
- •37.2 Is It Ever Too Early or Too Late to Needle a Bleb?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •37.5 Is It Better to Needle or Reoperate on a Failing Bleb?
- •Summary for the Clinician
- •References
- •38.1 Is One Tube Shunt Design Better than Another at Lowering IOP?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •39.1.1 Aqueous Shunts for Glaucoma (Supporting Evidence Level I/1c)
- •39.1.2 Cyclodestruction with Diode G-Probe (Supporting Evidence Level III/4)
- •39.1.3 Cyclodestruction with Diode Endocyclophotocoagulation (Supporting Evidence Level I/1c)
- •39.1.8 iScience (Canaloplasty) (Supporting Evidence III/4)
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •40.2 What Is the Ex-PRESS Mini-Shunt and How Does It Work?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •40.6 What Complications Are Specific to the Ex-PRESS Shunt Procedure?
- •Summary for the Clinician
- •References
- •41.1.1 When to Add a Trabeculectomy to Cataract Surgery
- •41.1.2 When to Add Phacoemulsification to a Trabeculectomy
- •Summary for the Clinician
- •41.2.1 Glaucoma as the Primary Problem
- •41.2.2 Cataract as the Primary Problem
- •Summary for the Clinician
- •41.3 How Is the Postoperative Course of a Phacotrabeculectomy Different than that After the Individual Surgeries?
- •Summary for the Clinician
- •References
- •42.1 What Is End-Stage Glaucoma?
- •Summary for the Clinician
- •42.2 Should I Operate on a Patient with End-Stage Glaucoma?
- •Summary for the Clinician
- •Summary for the Clinician
- •42.4 How Do Specific Complications of Surgery in End-Stage Glaucoma Lead to Vision Loss?
- •42.4.1 Hypotony Maculopathy
- •42.4.2 Retinal Detachment
- •42.4.3 Endophthalmitis
- •42.4.4 Malignant Glaucoma and others
- •Summary for the Clinician
- •42.5 What Can Be Done to Minimize Potential Vision Loss Due to Surgery in End-Stage Glaucoma?
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •Summary for the Clinician
- •43.3 What Is the Treatment of Choice in Normal-Tension Glaucoma – Medication, Laser, or Surgery?
- •Summary for the Clinician
- •43.4.1 Risk Factors for Progression in NTG
- •43.4.2 Disc Hemorrhage in NTG
- •Summary for the Clinician
- •References
- •Glaucomas: Pseudoexfoliation Glaucoma
- •44.1 Is There a Gene for Pseudoexfoliation Syndrome?
- •Summary for the Clinician
- •Summary for the Clinician
- •44.3 What Is the Risk of Developing Glaucoma Once PXF Material Is Observed in the Eye?
- •Summary for the Clinician
- •44.4.2 Cataract Extraction Technique
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •45.2 Is PDG Managed Differently than Primary Open Angle Glaucoma?
- •45.2.1 Medical Treatment
- •45.2.2 Trabeculoplasty
- •45.2.3 Trabeculectomy
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •45.6.1 Medical Therapy
- •45.6.2 Laser and Incisional Surgery
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Sturge Weber Syndrome
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Glaucoma and the Cornea
- •Summary for the Clinician
- •Summary for the Clinician
- •47.3 What Effect Does Laser Glaucoma Surgery Have on the Cornea?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Uveitic Glaucoma
- •Summary for the Clinician
- •48.2 Is There a Way to Distinguish Between Elevated IOP Due to a Steroid Response vs. Uveitis?
- •Summary for the Clinician
- •48.3 How Do Inflammation and Steroids Cause an Increase in IOP?
- •Summary for the Clinician
- •Summary for the Clinician
- •48.5 Is There a Preferred Surgery for Uveitic Glaucoma (Trabeculectomy vs. Tube vs. Laser)?
- •Summary for the Clinician
- •48.6 Is One Tube Preferred over Another in Uveitic Glaucoma?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Glaucomas: Neovascular Glaucoma
- •49.1.1 IOP Lowering Agents
- •49.1.3 Cycloplegics/Mydriatics
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •50.1 What Is the Best Way to Measure IOP in the Pediatric Patient?
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •51.1.1 Which Medications Can Be Used as First Line Agents in Children?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •52.1 How Do I Perform Goniosurgery?
- •52.1.2 What Can I Do Technically to Perform a Better Trabeculotomy ?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •53.2 Is Trabeculectomy Preferred over Tube Shunt Surgery in Children?
- •Summary for the Clinician
- •Summary for the Clinician
- •53.4 What Factors Help One Decide for or Against One Surgery over the Other?
- •Summary for the Clinician
- •53.5.1 In Trabeculectomy
- •53.5.2 In Tube-Shunts
- •Summary for the Clinician
- •Summary for the Clinician
- •53.7 What Can Be Done Technically to Perform a Better Glaucoma Drainage Device Surgery in Kids?
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Risk Factors
- •54.1 Who Is at Risk for Acute Angle-Closure?
- •54.1.1 What are the Anatomical Risk Factors?
- •54.1.2 Age, Gender and Ethnicity
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Iridotomy
- •55.1.1 Settings for Argon LPI
- •55.1.2 Settings for Nd-YAG LPI
- •Summary for the Clinician
- •Summary for the Clinician
- •55.3 If It Is Difficult to Penetrate the Iris, What Adjustments Can Be Made to the Laser Settings?
- •Summary for the Clinician
- •55.4.1 Visual Discomfort
- •55.4.2 Diplopia and/or Glare
- •55.4.3 Hemorrhage
- •55.4.4 Corneal Damage
- •55.4.5 Lens Damage
- •55.4.6 IOP Elevation
- •55.4.7 Progression of PAS Formation
- •55.4.8 Posterior Synechia
- •55.4.9 LPI Closure
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Imaging
- •Summary for the Clinician
- •56.2.1 Ultrasound Biomicroscopy (UBM)
- •56.2.3 Scheimpflug Photography
- •Summary for the Clinician
- •56.3 When Should UBM and AS-OCT Be Ordered: Is One Device Considered Better than the Other?
- •Summary for the Clinician
- •56.4.1 Qualitative Analysis
- •56.4.2 Quantitative Analysis
- •Summary for the Clinician
- •References
- •Angle-Closure Glaucoma: Medical Therapy
- •57.1.1 Carbonic Anhydrase Inhibitors
- •57.1.2 Beta-Blockers
- •57.1.3 Alpha-Agonists
- •57.1.4 Prostaglandin Analogs
- •57.1.5 Hyperosmotic Agents
- •57.1. 6 Miotics
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Complications: Hypotony
- •59.1 What are the Options in the Treatment of Early Postoperative Hypotony?
- •59.1.1 Compression Sutures
- •59.1.2 Anterior Chamber Reformation
- •59.1.3 Choroidal Drainage
- •59.1.4 Repairing Wound Leaks
- •59.1.5 Resuturing of Trabeculectomy Flap
- •Summary for the Clinician
- •59.2 If There Is Hypotony Maculopathy, What Should Be Done to Manage It?
- •59.2.1 Cataract Surgery and Hypotony
- •Summary for the Clinician
- •59.3 How Can I Manage Late Hypotony Due to a Scleral Melt?
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Complications: Bleb Leaks
- •60.1.2 With a Large/Brisk, Early Postoperative Bleb Leak, What Options Are Available to Help It Heal?
- •60.1.3 What Can I Do If the Leak Continues to Persist?
- •Summary for the Clinician
- •60.2.2 Autologous Blood Injection
- •60.2.3 Compression Sutures
- •60.2.4 Laser
- •60.2.5 Surgical Bleb Revision
- •Summary for the Clinician
- •Summary for the Clinician
- •References
- •Complications: Blebitis
- •Summary for the Clinician
- •Summary for the Clinician
- •61.3 How Do I Manage a Patient After the Blebitis Is Resolved?
- •Summary for the Clinician
- •References
- •Subject Index
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through the eye during phacoemulsification. These factors can increase the production of cytokines in the aqueous humor that stimulate the scarring process.
Whether to perform a limbus or fornix based conjunctival wound in phacotrabeculectomy is another common question. Similar long-term results are seen after either type of incision [23–25]. Although a fornixbased trabeculectomy allows better visualization during one-site cataract surgery, it is also associated with a higher risk of wound leakage. Generally after cataract surgery, a water-tight wound is desirable to decrease the risk of endophthalmitis; however, the trabeculectomy will lower eye pressure allowing the clear corneal wound to gape. In order to minimize this risk, corneal wounds should be sutured in combined two-site cases. Hypotony leading to shallow chambers can occur after phacotrabeculectomy, although the lens implant takes up less volume than a natural lens does and therefore lens-corneal touch may be less frequent. The use of releasable sutures constitutes an option to avoid hipotony in the early postoperative period (Fig. 41.2).
41.3.2 Postoperative Course
of a Phacotrabeculectomy vs. Phacoemulsification Alone
Visual recovery may be more prolonged with a greater incidence of postoperative refractive error following phacotrabeculectomy. It has been published that after phacotrabeculectomy, complete visual recovery may take up
to 6 weeks vs. 1 or 2 weeks at most with phacoemulsification alone. Chan et al. retrospectively evaluated the refraction of patients subjected to phacotrabeculectomy vs. phacoemulsification and found myopic refractive errors are more common after phacotrabeculectomy. The authors speculated that myopia was due to shallowing of the anterior chamber in a soft eye [26].
Usually combined cataract and glaucoma surgery is accompanied by a higher risk of intra and postoperative complications. Many of the complications associated with phacoemulsification may be particularly accen tuated in a combined surgery and may relate to increased inflammation, added surgical manipulation, wound integrity, and the presence of lens proteins associated with the cataract portion of the surgery [21].
Summary for the Clinician
››Following phacotrabeculectomy, there is in creased inflammation compared to trabeculectomy alone.
››Following phacotrabeculectomy, the postoperative course may be less predictable than after phacoemulsification alone (i.e., refractive errors).
››There may be an increased rate of intraoperative and postoperative complications following phacotrabeculectomy.
Acknowledgements Daniel Grigera, MD. Hospital Oftalmo logico Santa Lucia, Buenos Aires, Argentina. Virginia Zanutigh, MD. Centro Oftalmologico Quilmes, Buenos Aires, Argentina. The author appreciates the contributions, opinions, and recommendations of each of the above mentioned physicians.
Fig. 41.2 Phacotrabeculectomy: Two-site approach associated with releasable sutures Figure 2
References
1. Jampel H, Friedman D, Lubomski L, et al. (2002) Effect of technique on intraocular pressure after combined cataract and glaucoma surgery: An evidence-based review. Ophthal mology, 109, 2215–2224.
2. Kim D, Doyle J, Smith M. (1999) Intraocular pressure reduction following phacoemulsification cataract extraction with posterior chamber lens implantation in glaucoma patients. Ophthalmic Surg Lasers, 30, 37–40.
3. Friedman D, Jampel H, Lubomski L, et al. (2002) Surgical Strategies for coexisting glaucoma and cataract: An evidencebased Update. Ophthalmology, 109, 1902–1915.
4. Rich W, Cohan B. (1974) Early ocular hypertension after cataract extraction. Br J Ophthalmol, 58, 725–731.
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5. Shields M. (1989) Combined cataract extraction and glaucoma surgery. Ophthalmology, 89, 231–237
6. Shields M. (1986) Combined cataract extraction and guarded sclerectomy: Reevaluation in the extracapsular era. Ophthal mology, 93, 366–370.
7. Krupin T, Feitl M, Bishop K. (1989) Postoperative intraocular pressure rise in open angle glaucoma patients after cataract or combined cataract-filtration surgery. Ophthalmology, 96, 579–584.
8. Storr-Paulsen A, Bernth-Petersen P. (2001) Combined cataract and glaucoma surgery. Curr Opin Ophthalmol, 12, 41–46.
9. Storr-Paulsen A, Laugesen C. (1998) A prospective study of combined phacoemulsification-trabeculectomy versus con-
ventional phacoemulsification in cataract patients with coexisting open angle glaucoma. Acta Ophthalmol, 76, 696–699.
10.Hylton C, Friedman D, et al. (2003) Cataract after filtration surgery. Am J Ophthalmol, 135, 231–232.
11.AGIS Investigators (2001) The Advanced Glaucoma Intervention Study: 8. Risk of cataract formation after trabeculectomy. Arch Ophthalmol, 119, 1771–1779.
12.Lichter P, Musch D, Gillespie B, et al. (2001) Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery. Ophthalmology, 108, 1943–1953.
13.ChandrasekaranS,RochtchinaE,MitchellP.(2006)Associations between elevated intraocular pressure and glaucoma, use of glaucoma medications, and 5-year incident cataract: The Blue Mountains Eye Study. Ophthalmology, 113, 417–424.
14.Verges C, Cazal J, Lavin C. (2005) Surgical strategies in patients with cataract and glaucoma. Curr Opin Ophthalmol, 16, 44–52.
15.Lee R. (2004) Surgical management of coexisting cataract and glaucoma. Int Ophthalmol Clin, 44, 151–166.
16.Wishart P. (1993) Combined cataract extraction and trabeculectomy: Phacoemulsification compared with extracapsular technique. Ophthalmic Surg Lasers, 24, 814–821.
17.Shingleton B, Kuperwaser M. (1995) Comparison of combined cataract and glaucoma surgery using planned extracapsular and phacoemulsification techniques. Ophthalmic Surg Lasers, 26, 414–419.
18.Lochhead J, Salmon J. (2003) Long term effect on intraocular pressure of phacotrabeculectomy compared to trabeculectomy. Br J Ophthalmol, 87, 850–852.
19.Park H, Caprioli J. (1997) Temporal corneal phacoemulsification combined with superior trabeculectomy. A retrospective case-control study. Arch Ophthalmol, 115, 318.
20.Chang L, Thiagarajan M, Moseley M, et al. (2006) Intraocular pressure outcome in primary 5FU phacotrabeculectomies compared with 5FU trabeculectomies. J Glaucoma, 15, 475–481.
21.Heffelfinger B, Berman M, Krupin T, et al. (2000) Surgical management of coexisting glaucoma and cataract. Ophthal mol Clin North Am, 13, 545–551.
22.Siriwardena D, Minassian D, Dart J, et al. (2000) Anterior chamber flare after trabeculectomy and after phacoemulsification. Br J Ophthalmol, 84, 1056–1057.
23.Lemon L, Shin D, Kim C, et al. (1998) Limbus-based vs fornix-based conjunctival flap in combined glaucoma and cataract surgerv with adjunctive mitomycin C. Am J Ophthal mol, 125, 340–345.
24.Shingleton B, O’Donoghue M, et al. (1999) Phacotrabe culectomy: Limbus-based versus fornix-based conjunctival flaps in fellow eyes. Ophthalmology, 106, 1152–1155.
25.Tezel G, Kass M, et al. (1997) Comparative results of combined procedures for glaucoma and cataract: II: Limbusbased versus fornix-based conjunctival flaps. Ophthalmic Surg Lasers, 28, 551–557.
26.Chan J, Lai J, Tham C. (2006) Comparison of postoperative refractive outcome in phacotrabeculectomy and phacoemulsification with posterior chamber intraocular lens implantation. J Glaucoma, 15, 26–29.
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Surgery in End-Stage Glaucoma |
Fotis Topouzis
Core Messages
››In end-stage glaucoma patients there is higher likelihood of vision loss that will affect activities of daily living than in early glaucoma, therefore monitoring is more frequent and treatment decisions must be made more quickly.
››Target intraocular pressures in end-stage glaucoma are lower than in earlier stages of glaucoma.
››Surgery should be considered in end-stage glau coma if necessary.
››The “wipe-out” phenomenon describes an immediate postoperative unexplained vision loss and is a rare complication in end-stage glaucoma.
42.1 What Is End-Stage Glaucoma?
End-stage glaucoma is a term used to describe glaucoma that has reached a stage of extreme or near totalvision loss; however, there is no universally accepted formal definition. One definition implies that patients with end-stage glaucoma have a very constricted visual field, less than 10o in diameter [1]. According to the Advanced Glaucoma Intervention Study (AGIS) an AGIS visual field score of 17–20 classifies an eye as having end-stage glaucoma [2]. Others define end -stage
F. Topouzis
A’ Department of Ophthalmology, Aristotle University
of Thessaloniki, AHEPA Hospital, Stilponos Kyriakidi 1, 54636, Nea Efkarpia, 56403, Thessaloniki, Greece
e-mail: ftopouzis@otenet.gr
glaucoma based on a visual acuity (VA) of 20/200 or worse that is attributable to glaucoma [3].
There are several reasons why end-stage glaucoma patients should be evaluated and managed differently than those with earlier stages of the disease. Patients with end-stage glaucoma have a high risk of further disease progression [4]. Also, although peripheral vision is seriously affected in end-stage glaucoma, these patients may maintain good central vision. Furthermore, even with a visual acuity characterizing them as legally blind, it is possible for these patients to perform simple daily tasks [5]. Therefore, the preservation of this already seriously threatened vision is of major importance.
Performing visual field examination with reliable results may be difficult or in some cases impossible for patients with end-stage glaucoma. If only a central island of vision is spared and a visual field test can be performed, a central Humphrey 10-2 program may be more informative than 24-2 or 30-2 programs (on Octopus machine one would use the C08 program) [6]. End-stage glaucoma patients need more frequent monitoring of their remaining vision. In advanced glaucoma one does not have the luxury of a “wait and see” approach, as additional changes in visual field may be deleterious to central vision. Even small changes may be clinically significant. However, progression is very difficult to assess because small changes, possibly indi cating progression, can be difficult to differentiate from inter-test fluctuation [7].
In addition, it is difficult to assess changes in the optic disc when it presents with severe neuroretinal rim loss. In end-stage, very subtle and small neuroretinal rim changes may correspond to disproportionately significant changes in the visual acuity. For these reasons there may be less value in optic disc examination than in assessment of visual function at this stage of disease [8].
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Elevated intraocular pressure (IOP) is an identified risk factor for progression, and currently IOP reduction remains the only validated management approach to prevent progression [9, 10]. Individualization of glaucoma management involves the use of target IOP, which are based on a patient’s risk factors for progression, the level of IOP that caused damage, the severity of disease and patient’s expected longevity [11]. Target IOP should be set low in end-stage glaucoma.On the basis of literature target pressures seem to drop to lower and lower levels each decade [12].
Summary for the Clinician
››There is no universally accepted definition of end-stage glaucoma.
››End-stage glaucoma patients are managed differently than those patients with earlier stages of glaucoma.
››If only a central island of vision remains, visual field tests of the central degrees should be chosen.
››Assessing a nerve with very advanced neuroretinal rim loss may not provide useful information in terms of monitoring for progression.
››IOP target should be much lower in end stage glaucoma.
42.2 Should I Operate on a Patient with End-Stage Glaucoma?
Glaucoma procedures are required for the prevention of visual field loss when further IOP reduction is needed despite maximum medical therapy [13]. In cases of unre liable visual fields or inability to perform a visual field examination, visual acuity loss or a patient’ s perception of vision decline may be critical in our decision to surgically intervene, as there is a strong association between some types of perceived visual deterioration and measured bilateral visual field deterioration [14].
Deciding whether to operate on such patients depends on an evaluation of the benefits and risks of such an action. First, one must assess whether medical therapy is failing to reach the target IOP [15]. To prevent progression IOP needs to be consistently low [16]. It has been suggested recently that large IOP fluctuation is
one of the strongest risk factors for progression of glau comatous damage [17–23], though there are still contro versies in the literature concerning this issue [24, 25]. Trabeculectomy has been reported to be associated with less diurnal IOP fluctuation compared to maximum medical therapy in patients with advanced glaucoma [26, 27].
There are specific characteristics of end-stage eyes that could make surgical intervention difficult and endanger the outcome. Eyes with end-stage glaucoma are likely to have undergone previous operations (glaucoma or cataract) and/or to have used topical glaucoma drugs for a long time, both of which may have negative effects on the conjunctiva, and therefore, on the outcome of a new operation [28–31].
The surgical options are the same as for earlier stages of glaucoma. Trabeculectomy with antimetabolites effectively reduces IOP compared to trabeculectomy alone, as well as the risk of surgical failure in eyes with or without previous surgery [32–35]. Alternatively, glaucoma drainage implants are indicated for cases in which glaucoma filtration surgery has failed or for cases of refractory glaucomas (neovascular, uveitic, other secondary open-angle and angle-closure glaucomas) which do not respond well to standard filtration surgery [36–38]. Nonpenetrating glaucoma surgery may also be considered [39], however, given the low levels of IOP needed in end-stage glaucoma [10, 16], a trabeculectomy with antimetabolite may more reliably achieve the desired pressure [40].
Cycloablation is yet another option in the form of cyclophotocoagulation (transscleral or endoscopic) or cyclocryotherapy. Traditionally, cycloablation has been reserved for eyes with poor vision to prevent pain from high IOP or for those with significant conjunctival scarring [41–43]. Recent studies have suggested that cycloablation can be used as an alternative approach to incisional surgery in the treatment of primary openangle and pseudoexfoliative glaucoma [44, 45], as well as for chronic angle-closure glaucoma [46]. Cyclocryother apy has similar indications for implementation [47, 48]. However, it must be stated that the visual outcomes after cycloablation in patients with end-stage glaucoma and only a small island of central vision have not been fully studied.
Finally, one can consider the option of withholding surgery if central fixation has already been lost. It is essential to discuss with the patient the benefits vs. the costs and risks of all management options.
