- •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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other causes of optic neuropathy or visual field loss. Unless the practitioner is comfortable with performing a full neuro-ophthalmological evaluation and ordering appropriate investigations on this basis, he/she should request a consultation from a neuro-ophthalmologist. This ensures that neuro-imaging studies will be properly directed by the physical findings of the entire visual system.
Summary for the Clinician
››Cupping is a key feature of glaucomatous optic neuropathy but can also be found in other optic neuropathies.
››Dilated disc examination is required to provide an adequate binocular view for stereoscopic assessment of cup depth and distribution of pallor, and to facilitate slit-lamp measurement of vertical disc diameter and cup-to-disc ratio.
››Measure overall disc size (vertical disc diameter) to provide a context for the cup size - large discs may have physiologically large cups while small discs may have small cups which carry the possibility of masking changes we more classically associate with glaucomatous damage.
››Physiologically large cups may be normal in large discs but this can only be diagnosed with certainty in retrospect, when there has been no glaucomatous change over a period of time.
››Monitoring for change over a time period may ultimately be the only way to distinguish between glaucomatous pathology vs. individual anatomy in patients with large discs.
››Although the base of the cup in glaucomatous optic neuropathy is pale, giving the impression of optic disc pallor, the remaining neuroretinal rim maintains its yellow-pink color. In the absence of other pathology, a glaucoma disc should not be described as “pale.”
››Pallor of the neuroretinal rim should prompt the clinician to consider nonglaucomatous causes of the disc changes and field loss.
››If visual field loss does not correlate with glaucomatous features on disc examination, suspect another etiology and request assistance from an appropriate specialist.
References
1. Park KH, Tomita G, Liou SY, et al. (1996) Correlation between peripapillary atrophy and optic nerve damage in normaltension glaucoma. Ophthalmology 103(11): 1899–906.
2. Jonas JB, Nguyen XN, Gusek GC, et al. (1989) Parapapillary chorioretinal atrophy in normal and glaucoma eyes. I. Morpho metric data. Invest Ophthalmol Vis Sci 30(5): 908–18.
3. Kubota T, Jonas JB, Naumann GO (1993) Direct clinico-his- tological correlation of parapapillary chorioretinal atrophy. Br J Ophthalmol 77(2): 103–6.
4. Jonas JB, Gusek GC, Fernandez MC (1991) Correlation of the blind spot size to the area of the optic disk and parapapillary atrophy. Am J Ophthalmol 111(5): 559–65.
5. Jonas JB, Bergua A, Schmitz-Valckenberg P, et al. (2000) Ranking of optic disc variables for detection of glaucomatous optic nerve damage. Invest Ophthalmol Vis Sci 41(7): 1764–73.
6. Emdadi A, Kono Y, Sample PA, et al. (1999) Parapapillary atrophy in patients with focal visual field loss. Am J Ophthalmol 128(5): 595–600.
7. Jonas JB, Martus P, Horn FK, et al. (2004) Predictive factors of the optic nerve head for development or progression of glaucomatous visual field loss. Invest Ophthalmol Vis Sci 45(8): 2613–8.
8. Uchida H, Ugurlu S, Caprioli J (1998) Increasing peripapillaryatrophyisassociatedwithprogressiveglaucoma .Ophthal mology 105(8): 1541–5.
9. Apple DJ, Rabb MF, Walsh PM (1982) Congenital anomalies of the optic disc. Surv Ophthalmol 27(1): 3–41.
10.Grodum K, Heijl A, Bengtsson B (2001) Refractive error and glaucoma. Acta Ophthalmol Scand 79(6): 560–6.
11.Mitchell P, Hourihan F, Sandbach J, et al. (1999) The relationship between glaucoma and myopia: the Blue Mountains Eye Study. Ophthalmology 106(10): 2010–5.
12.Chihara E, Liu X, Dong J, et al. (1997) Severe myopia as a risk factor for progressive visual field loss in primary openangle glaucoma. Ophthalmologica 211(2): 66–71.
13.Curcio CA, Saunders PL, Younger PW, et al. (2000) Peri papillary chorioretinal atrophy: Bruch’s membrane changes and photoreceptor loss. Ophthalmology 107(2): 334–43.
14.Votruba M, Thiselton D, Bhattacharya SS (2003) Optic disc morphology of patients with OPA1 autosomal dominant optic atrophy. Br J Ophthalmol 87(1): 48–53.
15.Dorrell D (1978) The tilted disc. Br J Ophthalmol 62(1): 16–20.
16.Tong L, Saw SM, Chua WH, et al. (2004) Optic disk and retinal characteristics in myopic children. Am J Ophthalmol 138(1): 160–2.
17.Giuffre G (1991) Chorioretinal degenerative changes in the tilted disc syndrome. Int Ophthalmol 15(1): 1–7.
18.Jonas JB, Kling F, Grundler AE (1997) Optic disc shape, corneal astigmatism, and amblyopia. Ophthalmology 104(11): 1934–7.
19.Vongphanit J, Mitchell P, Wang JJ (2002) Population prevalence of tilted optic disks and the relationship of this sign to refractive error. Am J Ophthalmol 133(5): 679–85.
20.Tong L, Chan YH, Gazzard G, et al. (2007) Heidelberg retinal tomography of optic disc and nerve fiber layer in singapore children: variations with disc tilt and refractive error. Invest Ophthalmol Vis Sci 48(11): 4939–44.
72 |
B. Edmunds and J. C. Morrison |
|
|
21.Tay E, Seah SK, Chan SP, et al. (2005) Optic disk ovality as an index of tilt and its relationship to myopia and perimetry. Am J Ophthalmol 139(2): 247–52.
22.Vuori ML, Mantyjarvi M (2007) Tilted disc syndrome and colour vision. Acta Ophthalmol Scand 85(6): 648–52.
23.Saw SM, Tong L, Chua WH, et al. (2005) Incidence and progression of myopia in Singaporean school children. Invest Ophthalmol Vis Sci 46(1): 51–7.
24.Vuori ML, Mantyjarvi M (2008) Tilted disc syndrome may mimic false visual field deterioration. Acta Ophthalmol Scand 86(6): 622–65.
25.Brazitikos PD, Safran AB, Simona F, et al. (1990) Threshold perimetry in tilted disc syndrome. Arch Ophthalmol 108(12): 1698–700.
26.Park KH, Caprioli J (2002) Development of a novel reference plane for the Heidelberg retina tomograph with optical coherence tomography measurements. J Glaucoma 11(5): 385–91.
27.Yamazaki Y, Yoshikawa K, Kunimatsu S, et al. (1999) Influ ence of myopic disc shape on the diagnostic precision of the Heidelberg Retina Tomograph. Jpn J Ophthalmol 43(5): 392–7.
28.Yu S, Tanabe T, Hangai M, et al. (2006) Scanning laser polarimetry with variable corneal compensation and optical coherence tomography in tilted disk. Am J Ophthalmol 142(3): 475–82.
29.DoshiA,KreidlKO,LombardiL,etal.(2007)Nonprogressive glaucomatous cupping and visual field abnormalities in young Chinese males. Ophthalmology 114(3): 472–9.
30.Boyce SW, Platia EV, Green WR (1978) Drusen of the optic nerve head. Ann Ophthalmol 10(6): 695–704.
31.Friedman AH, Beckerman B, Gold DH, et al. (1977) Drusen of the optic disc. Surv Ophthalmol 21(5): 373–90.
32.Tso MO (1981) Pathology and pathogenesis of drusen of the optic nerve head. Ophthalmology 88(10): 1066–80.
33.Auw-Haedrich C, Staubach F, Witschel H (2002) Optic disk drusen. Surv Ophthalmol 47(6): 515–32.
34.Mullie MA, Sanders MD (1985) Scleral canal size and optic nerve head drusen. Am J Ophthalmol 99(3): 356–9.
35.Jonas JB, Gusek GC, Guggenmoos-Holzmann I, et al. (1987) Optic nerve head drusen associated with abnormally small optic discs. Int Ophthalmol 11(2): 79–82.
36.Spencer WH (1978) Drusen of the optic disk and aberrant axoplasmic transport. The XXXIV Edward Jackson memorial lecture. Am J Ophthalmol 85(1): 1–12.
37.Floyd MS, Katz BJ, Digre KB (2005) Measurement of the scleral canal using optical coherence tomography in patients with optic nerve drusen. Am J Ophthalmol 139(4): 664–9.
38.Spencer TS, Katz BJ, Weber SW, et al. (2004) Progression from anomalous optic discs to visible optic disc drusen. J Neuroophthalmol 24(4): 297–8.
39.Sacks JG, O’Grady RB, Choromokos E, et al. (1977) The pathogenesis of optic nerve drusen. A hypothesis. Arch Ophthal mol 95(3): 425–8.
40.Lorentzen SE (1966) Drusen of the optic disk. A clinical and genetic study. Acta Ophthalmol (Copenh) Suppl 90: 1–180.
41.Mustonen E (1983) Pseudopapilloedema with and without verified optic disc drusen. A clinical analysis II: visual fields. Acta Ophthalmol (Copenh) 61(6): 1057–66.
42.Katz BJ, Pomeranz HD (2006) Visual field defects and retinal nerve fiber layer defects in eyes with buried optic nerve drusen. Am J Ophthalmol 141(2): 248–253.
43.Wilkins JM, Pomeranz HD (2004) Visual manifestations of visible and buried optic disc drusen. J Neuroophthalmol 24(2): 125–9.
44.Savino PJ, Glaser JS, Rosenberg MA (1979) A clinical analysis of pseudopapilledema. II. Visual field defects. Arch Ophthalmol 97(1): 71–5.
45.Cohen DN (1971) Drusen of the optic disc and the development of field defects. Arch Ophthalmol 85(2): 224–6.
46.Lansche RK, Rucker CW (1957) Progression of defects in visual fields produced by hyaline bodies in optic disks. AMA Arch Ophthalmol 58(1): 115–21.
47.Lee AG, Zimmerman MB (2005) The rate of visual field loss in optic nerve head drusen. Am J Ophthalmol 139(6): 1062–6.
48.Roh S, Noecker RJ, Schuman JS, et al. (1998) Effect of optic nerve head drusen on nerve fiber layer thickness. Oph thalmology 105(5): 878–85.
49.Mistlberger A, Sitte S, Hommer A, et al. (2001) Scanning laser polarimetry (SLP) for optic nerve head drusen. Int Ophthalmol 23(4–6): 233–7.
50.Tatlipinar S, Kadayifcilar S, Bozkurt B, et al. (2001) Polarimetric nerve fiber analysis in patients with visible optic nerve head drusen. J Neuroophthalmol 21(4): 245–9.
51.Kurz-Levin MM, Landau K (1999) A comparison of imaging techniques for diagnosing drusen of the optic nerve head. Arch Ophthalmol 117(8): 1045–9.
52.Mustonen E, Kallanranta T, Toivakka E (1983) Neurological findings in patients with pseudopapilloedema with and without verified optic disc drusen. Acta Neurol Scand 68(4): 218–30.
53.Broman AT, Quigley HA, West SK, et al. (2008) Estimating the rate of progressive visual field damage in those with open -angle glaucoma, from cross-sectional data. Invest Ophthalmol Vis Sci 49(1): 66–76.
54.Foster PJ, Buhrmann R, Quigley HA, et al. (2002) The definition and classification of glaucoma in prevalence surveys. Br J Ophthalmol 86(2): 238–42.
55.Araie M, Sekine M, Suzuki Y, et al. (1994) Factors contributing to the progression of visual field damage in eyes with normal-tension glaucoma. Ophthalmology 101(8): 1440–4.
56.Tezel G, Siegmund KD, Trinkaus K, et al. (2001) Clinical factors associated with progression of glaucomatous optic disc damage in treated patients. Arch Ophthalmol 119(6): 813–8.
57.Gordon MO, Beiser JA, Brandt JD, et al. (2002) The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 120(6): 714–20; discussion 829–30.
58.JonasJB,ZachFM,GusekGC,etal.(1989)Pseudoglaucomatous physiologic large cups. Am J Ophthalmol 107(2): 137–44.
59.Lichter PR (1976) Variability of expert observers in evaluating the optic disc. Trans Am Ophthalmol Soc 74: 532–72.
60.Carpel EF, Engstrom PF (1981) The normal cup-disk ratio. Am J Ophthalmol 91(5): 588–97.
61.Varma R, Steinmann WC, Scott IU (1992) Expert agreement in evaluating the optic disc for glaucoma. Ophthalmology 99(2): 215–21.
62.Garway-Heath DF, Ruben ST, Viswanathan A, et al. (1998) Vertical cup/disc ratio in relation to optic disc size: its value
7 Optic Nerve: Atypical Nerves and Nerve Findings |
73 |
|
|
in the assessment of the glaucoma suspect. Br J Ophthalmol 82(10): 1118–24.
63.Healey PR, Mitchell P, Smith W, et al. (1997) Relationship between cup-disc ratio and optic disc diameter: the Blue Mountains Eye Study. Aust N Z J Ophthalmol 25(Suppl 1): S99–101.
66.Tielsch JM, Sommer A, Katz J, et al. (1991) Racial variations in the prevalence of primary open-angle glaucoma. The Baltimore Eye Survey. JAMA 266(3): 369–74.
67.Mason RP, Kosoko O, Wilson MR, et al. (1989) National survey of the prevalence and risk factors of glaucoma in St. Lucia, West Indies. Part I. Prevalence findings. Ophthalmology 96(9):
64.JonasJB,BuddeWM,Panda-JonasS(1999)Ophthalmoscopic 1363–8.
evaluation of the optic nerve head. Surv Ophthalmol 43(4): 68. Mardin CY, Horn FK (1998) Influence of optic disc size on
293–320.
65.Varma R, Tielsch JM, Quigley HA, et al. (1994) Race-, age-, gender-, and refractive error-related differences in the normal optic disc. Arch Ophthalmol 112(8): 1068–76.
the sensitivity of the Heidelberg Retina Tomograph. Graefes Arch Clin Exp Ophthalmol 236(9): 641–5.
69.Funaki S, Shirakashi M, Abe H (1998) Relation between size of optic disc and thickness of retinal nerve fibre layer in normal subjects. Br J Ophthalmol 82(11): 1242–5.
