- •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
236 |
A. L. Jamil and R. P. Mills |
|
|
Summary for the Clinician
››Every follow-up visit with a glaucoma patient is a chance to underscore the importance of regular use of prescribed medications.
››Education is empowers the patient. Educational brochures and videos are useful. Have your office staff instruct patients on how to instill drops and watch them to ensure that they are doing it properly.
››Your office can provide dated medication schedules to help confused patients. Suggest linking medications to habitual daily activities.
››Simplify drug regimens as much as possible through once daily medications and combination drugs.
››Local support groups should be offered to patients to help them cope with glaucoma and to exchange ideas on how to use their medi cations.
››Table 30.3 provides ideas to help augment patient compliance.
References
1. Berg JS, Dischler J, Wagner DJ, Raja JJ, Palmer-Shevlin N. Medication compliance: a healthcare problem. Ann Pharma cother. 1993;27(Suppl 9):S1–24.
2. Dawn AG, Santiago-Turla C, Lee PP. Patient expectations regarding eye care focus group results. Arch Ophthalmol. 2003;121:762–8.
3. Friedman DS, Quigley HA, Gelb L, et al. Using pharmacy claims data to study adherence to glaucoma medications: methodology of the glaucoma adherence and persistence study (GAPS). Invest Ophthalmol Vis Sci. 2007;48:5052–7.
4. Herndon LW, Brunner TM, Rollins JN. The glaucoma research foundation pa tient survey: patient understanding of glaucoma and its treatment. Am J Ophthalmol. 2006;141: S22–7.
5. Jackevicius CA, Mamdani M, Tu JV. Adherence in statin therapy in elderly patients with and without acute coronary syndrome. JAMA. 2002;288:462–7.
6. Kass MA, Heuer DK, Higginbotham EJ, et al.; For Ocular Hypertension Treatment Study Group. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120(6):701–13.
7. Kass MA, Meltzer DW, Gordon M, et al. Compliance with topical pilocarpine treatment. Am J Ophthalmol. 1986;101: 515–23.
8. Kosoko O, Quigley HA, Vitale S, et al. Risk factors for noncompliance with glaucoma follow-up visits. Ophthalmology. 1998;105:2105–11.
9. Levy G, Zamacona MK, Jusko WJ. Developing compliance
instructions for drug labeling. Clin Pharmacol Ther. 2000; 68:586–91.
10.McDonnell PJ, Jacobs MR. Hospital admissions resulting from preventable adverse drug reactions. Ann Pharmacother. 2002;36:1331–6.
11.Nordstrom B, Friedman D, Mozaffari E, Quigley H, Walker
A.Persistence and adherence with topical glaucoma therapy. Am J Ophthalmol. 2005;140:598–606.
12.Osterberg L, Blaschke T. Adherence to medication. N Engl
JMed. 2005;353:487–95.
13.Owsley C, McGwin G, Scilley K, et al. Perceived barriers to care and attitudes about vision and eye care: focus groups with older African Americans and eye care providers. Invest Ophthalmol Vis Sci. 2006;47:2797–802.
14.Patel SC, Spaeth GL. Compliance in patients prescribed eyedrops for glaucoma. Ophthal Surg. 1995;26:233–6.
15.Reardon G, Schwartz GF, Mozaffari E. Patient persistency with topical ocular hypotensive therapy in a managed care population. Am J Ophthalmol. 2004;137(Suppl 1):S3–12.
16.Senst BL, Achusim LE, Genest RP, et al. Practical approach to determining costs and frequency of adverse drug events in a health care network. Am J Health Syst Pharm. 2001;58: 1126–32.
17.Sloan FA, Brown DS, Carlisle ES, et al. Monitoring visual status: why patients do or do not comply with practice guidelines. Health Serv Res. 2004;39:1429–48.
18.Stewart WC, Konstas AG, Pfeiffer N. Patient and ophthalmologist attitudes concerning compliance and dosing in glaucoma treatment. J Ocul Pharmacol Ther. 2004;20: 461–9.
19.Tsai JC, McClure CA, Ramos SE, Schlundt DG, Pichert JW. Compliance barriers in glaucoma: a systematic classification. J Glaucoma. 2003;12:393–8.
Medical Treatment: Alternative Medicine |
31 |
and Glaucoma |
Louis R. Pasquale
Core Messages
››When patients inquire about the relationship between lifestyle factors and glaucoma the physician should seize upon this interaction to educate them about their disease.
››Any alternative treatment for glaucoma should, at the very least, do no harm and not detract from conventional measures to manage the condition.
››There may be activities to avoid for glaucoma patients, although more work is needed to determine if these activities predispose to glaucoma or contribute to the progression of the pre-existing disease.
››The Ocular Hypertension Treatment Study is the only trial that demonstrates the efficacy of a strategy to primarily prevent primary openangle glaucoma (POAG). There are no other proven alternative strategies to prevent the development of POAG.
››The Collaborative Normal Tension Glaucoma Study and the Early Manifest Glaucoma Study are the only trials that demonstrate the efficacy of a strategy to favorably alter the natural history of open-angle glaucoma (OAG). There are no other proven strategies to prevent the progression of OAG.
L.R. Pasquale
Department of Ophthalmology, Harvard Medical School,
243 Charles Street, Boston, MA 02114, USA
e-mail: Louis_Pasquale@meei.harvard.edu
31.1 Is There Anything the Patient
Can Do to Improve the Outcome
of Their Disease Besides Using
Conventional Treatments
(Medications and Surgery)?
When patients ask this sort of a question, seize this opportunity to bond with them. Do not dismiss such a question in a trivial manner. Such a question typically comes from newly diagnosed glaucoma patients who are in the initial phases of acquiring knowledge about their condition and learning about you, the physician. The question is usually not meant to challenge your knowledge about glaucoma. Use this question as a stepping-stone to explain the natural history of glaucoma and what one can expect from conventional therapy. If the patient senses an aloof approach from you, how will they respond if you actually recommend something invasive like a trabeculectomy, even when such a recommendation is totally appropriate? Glaucoma is a life-long condition and providing knowledgeable answers to this type of question will go a long way toward building a healthy patient–physician relationship.
When considering your response to this question, realize that you cannot dismiss an unconventional therapy that a patient may inquire about simply because there is no data that addresses the question. Relatively speaking, there are very few randomized clinical trials (RCTs) that assess the role of conventional therapy vs. observation in glaucoma. The Ocular Hypertension Treatment Study is the only RCT that assesses whether a specific strategy (lowering intraocular pressure (IOP)) prevents glaucoma and this study was performed in a population that was at high risk for developing primary open-angle glaucoma (POAG) by virtue of having
J. A. Giaconi et al. (eds.), Pearls of Glaucoma Management, |
237 |
DOI: 10.1007/978-3-540-68240-0_31, © Springer-Verlag Berlin Heidelberg 2010 |
|
238 |
L. R. Pasquale |
|
|
elevated IOP at baseline [1]. The European Glaucoma Prevention Study was the only other glaucoma primary prevention trial and it was placebo-controlled. It showed that when IOP lowering was limited to a specific agent (dorzolamide 2%), one could not prevent POAG among patients with ocular hypertension [2]. The only RCTs that assessed the role of conventional therapy in retarding disease progression are The Collab orative Normal Tension Glaucoma Study [3] and the Early Manifest Glaucoma Trial [4]. Collectively these two studies showed that lowering IOP with medicine, laser trabeculoplasty or incisional surgery favorably alters the natural progression of open-angle glaucoma (OAG) that occurred across a spectrum of IOP. The other glaucoma RCTs assessed, if one form of IOPlowering therapy was superior to another in the management of the disease (the relevant trials include The Glaucoma Laser Trial [5], The Advanced Glaucoma Intervention Study [6], The Collaborative Initial Glau coma Treatment Study [7]). There are no RCTs to demonstrate if any strategy, conventional or otherwise, prevents glaucoma in a population that is not at a high risk of developing the disease.
To provide a comprehensive answer to this question one must also consider that certain lifestyle activities may elevate IOP and there are hints some of these activities could predispose to POAG in subsets of patients. Patients rarely look at the issue of lifestyle and glaucoma from this perspective. It is reasonable for clinicians to be aware of lifestyle activities that elevate IOP and understand the magnitude and duration of their ocular hypertensive effect and their potential impact on glaucoma. For example, playing high wind musical instruments that require the generation of high intrathoracic pressures can produce an IOP that is double the baseline level in a short time period [8]. Luckily IOP returns to baseline fairly quickly after playing ceases. Nonetheless, it is theoretically possible that if someone plays an instrument such as the saxophone regularly for prolonged time periods, a clinically significant increase in IOP could result. While there is no strong evidence that playing these instruments predisposes to glaucoma, it is reasonable to alert a glaucoma patient who happens to play these instruments of this effect, particularly if the patient is developing progressive disease at seemingly normal IOP.
Along a similar theme, certain yoga exercises that place the eye below the heart causes an increase in IOP
that is quite alarming [9]. As soon as the subject assumes a normal posture the IOP returns to baseline. Many glaucoma specialists have anecdotally noted cases of “normal tension glaucoma” in which a careful history revealed frequent performance of inverted position yoga exercises. These anecdotes are supported by published reports of glaucoma progression among yoga practitioners [10, 11]. Figure 31.1 illustrates the documentation of an IOP rise during a headstand performed by a yoga instructor. This particular patient sought an alternative medical opinion to confirm a diagnosis of normal tension glaucoma. In the seated position, her IOP was 10 mmHg, OU but increased to 50 mmHg OU while assuming an inverted position. Ophthalmic examination revealed glaucomatous cupping and corresponding visual field deficits. After
Fig. 31.1 Documentation of IOP readings with a Perkins tonometer in a yoga instructor with presumed “normal tension glaucoma.” This patient sought several opinions regarding glaucoma before it was discovered that she was a yoga instructor. IOP while seated was 10 mmHg but rose to 50 mmHg during inverted posture. Treatment with medical therapy blunted the IOP during head down posture positions (case courtesy of Dr. Oscar Albis, Asociación para Evitar la Ceguera en México)
31 Medical Treatment: Alternative Medicine and Glaucoma |
239 |
|
|
initiating bimatoprost 0.004% nightly, IOP with inverted posture was in the mid-twenties and there has been no progressive optic nerve or visual field change after 4 years of follow-up. While the well-documented effect of increased IOP after assuming an inverted posture and case reports suggesting visual field worsening in yoga practitioners are intriguing, observational studies linking inverted yoga exercises and POAG are lacking. However, it pays to warn glaucoma patients about IOP elevations that are associated with inverted posture positions. Furthermore, physicians should consider prolonged performance of such activities as an occasional cause of “normal tension glaucoma” or disease progression despite seemingly excellent IOP control.
Caffeine or trimethylxanthine is a commonly ingested CNS stimulant that is generally regarded as safe by the FDA. Caffeine is consumed by a high percentage of the general public and there is generally, a fairly wide spread overall consumption reported in the general population. Caffeine is an adenosine receptor antagonist and adenosine receptors are involved in aqueous humor dynamics [12, 13]. Most studies [14–18] with some exceptions [19, 20] demonstrate that after caffeine consumption from beverages such as caffeinated coffee there is a modest increase of IOP (~2 mmHg) that lasts for about 2 h. In a large prospective observational study, Kang and colleagues found that while caffeine consumption did not increase risk of POAG, overall, there was an increased risk for high tension POAG among those with a positive family history of glaucoma [21]. While this finding requires confirmation, it suggests that POAG subjects with a family history for the disease may want to examine their caffeine consumption pattern as a way to modify their IOP while also adhering to conventional therapy as suggested by their treating ophthalmic physician.
Summary for the Clinician
››When patients ask about alternative therapies for their glaucoma it should be looked upon as an opportunity to educate the patient about glaucoma.
››Certain lifestyle choices – playing high-resistance wind instruments, practicing Yoga, and consuming caffeine – may have effects on IOP.
31.2 When a Patient Asks About
the Effect of Lifestyle on Glaucoma, How Can I Answer this with Regard to Exercise, Smoking, Alcohol,
and Diet?
There are many studies regarding how specific lifestyle factors affect IOP and there are some high quality cross sectional and prospective studies that assess the relation between selected lifestyle behaviors and OAG. Indisputably IOP is a strong risk factor for OAG and modifying IOP with conventional therapy can alter the natural course of the disease. Thus another objective in addressing patient-related questions regarding lifestyle and glaucoma, is, to be generally knowledgeable of the literature regarding the relation between specific lifestyle behaviors, IOP and glaucoma. Of course, in the absence of clinical trials, one needs to be cautious about the conclusions that can be reached from such observational studies. The literature for each of these lifestyles activities is summarized briefly below. Also specific recommendations regarding these activities in glaucoma are provided based on the existing evidence.
31.2.1 Exercise
Patients with glaucoma will frequently ask whether aerobic exercise is “good for glaucoma.” There is strong evidence that aerobic exercise lowers IOP [22–26]. Furthermore, people who are more conditioned to regular strenuous activity have lower IOP than their sedentary counterparts [27]. Isometric exercise like lifting weights may produce a small IOP increase during exertion [28] that is followed by a modest decline in IOP [29]. Currently there are no cohort studies that have evaluated the relation between exercise in any form and glaucoma. Nonetheless, moderate aerobic exercise has many health benefits and should be encouraged. Physicians often wonder if exercise will induce significant IOP elevation in pigmentary glaucoma patients, but the literature suggests this concern is not supported [30, 31]. Of course, if a pigmentary glaucoma patients report symptoms consistent
