- •Preface
- •Contents
- •1.1.1 The Vitreous
- •1.1.1.1 Embryology
- •1.1.1.2 The Anatomy
- •1.1.1.3 Anatomical Attachments of the Vitreous to the Surrounding Structures
- •1.1.2 The Retina
- •1.1.2.1 Embryology
- •1.1.2.2 Anatomy
- •Retinal Pigment Epithelium (RPE)
- •Photoreceptor Layer
- •Intermediary Neurones
- •Ganglion Cells
- •Retinal Blood Vessels
- •Other Fundal Structures
- •1.1.3 The Physiology of the Vitreous
- •1.2 Clinical Examination and Investigation
- •1.2.1 Using the Database
- •1.2.2 Examination of the Eye
- •1.2.2.1 Examination Technique
- •Visual Acuity
- •1.2.2.2 The Slit Lamp
- •1.2.2.3 Binocular Indirect Ophthalmoscope
- •1.2.2.4 Using the Indenter
- •1.2.2.5 Ultrasonography
- •Posterior Vitreous Detachment (PVD)
- •Retinal Tear
- •Retinal Detachment
- •Subretinal Haemorrhage
- •Retinoschisis
- •Choroidal Elevation
- •Trauma
- •1.2.2.6 Optical Coherence Tomography
- •Time-Domain OCT
- •Colour Coding
- •Frequency-Domain OCT
- •Full-Field OCT
- •Scan Resolution
- •Images and Measurements
- •Performing the Scan
- •Macular Scan Patterns
- •Central Retinal Thickness
- •Inner Segment and Outer Segment Junction and External Limiting Membrane
- •1.2.3 Subjective Tests
- •1.2.4 The Preoperative Assessment
- •1.3 Summary
- •References
- •2: Introduction to Vitreoretinal Surgery
- •2.1 Introduction
- •2.2 Choice of Anaesthesia
- •2.3 Pars Plana Vitrectomy
- •2.3.1 Sclerotomies
- •2.3.2 Where to Place the Sclerotomies
- •2.3.3 Securing the Infusion Cannula
- •2.3.4 Checking the Infusion
- •2.3.6 The Superior Sclerotomies
- •2.3.6.1 Where to Place
- •2.3.7 Checking the View
- •2.3.8 The Independent Viewing System
- •2.3.9 Removing the Vitreous
- •2.4 Vitrectomy Cutters
- •2.5 Handling the Light Pipe
- •2.6 Use of Sclerotomy Plugs
- •2.7 The Internal Search
- •2.8 Endolaser
- •2.9 Using a Contact Lens
- •2.10 Maintaining a View
- •2.10.1 Microscope
- •2.10.3 Cornea
- •2.10.4 Blood in the Anterior Chamber
- •2.10.5 Condensation on an Intraocular Lens Implant
- •2.10.6 Cataract Formation
- •2.10.7 Pupillary Dilation
- •2.11 Closing
- •2.12 Peroperative Complications
- •2.12.1 Iatrogenic Breaks
- •2.12.1.1 Causes
- •2.12.2 Choroidal Haemorrhage
- •2.12.3 Haemorrhage from Retinal or Other Blood Vessels
- •2.12.4 Lens Touch
- •2.12.5 Hypotony
- •2.13 Postoperative Complications
- •2.13.1 Cataract
- •2.13.2 Endophthalmitis
- •2.13.3 Corneal Changes
- •2.13.4 Choroidal Haemorrhage
- •2.13.5 Raised Intraocular Pressure
- •2.13.6 Retinal Breaks and RRD
- •2.13.7 Hypotony
- •2.13.8 Scleritis
- •2.13.9 Sympathetic Uveitis
- •2.14 Adjustments for 20 Gauge Vitrectomy
- •2.14.1 Construction of Superior Sclerotomies
- •2.14.2 Priming
- •2.14.3 Self-Sealing Sclerotomies
- •2.15 Adjustments for 23 and 25 Gauge Vitrectomy
- •2.15.1 Instrumentation
- •2.15.2 Surgical Technique
- •2.15.2.1 Vitrectomy Technique
- •2.15.3 Flexibility
- •2.15.4 Indentation
- •2.15.5 Flow Rates
- •2.15.6 Trochar Internal Protrusion
- •2.15.7 Silicone Oil
- •2.16 Complications
- •2.16.1 Peroperative
- •2.16.1.1 Extrusion of the Trochar on Removal of Instrumentation
- •2.16.1.2 Conjunctival Chemosis
- •2.16.1.3 Hypotony
- •2.16.1.4 Endophthalmitis
- •2.16.2 Postoperative Retinal Break Formation
- •2.17 Advantages and Disadvantages of 23 and 25 G Systems
- •2.18 Combined Cataract Extraction and PPV
- •2.18.1 How to Decide Whether to Perform Combined Surgery
- •2.18.1.1 Accommodation
- •2.19 Biometry
- •2.20 Chandelier Systems and Bimanual Surgery
- •2.20.1 Possible Complications
- •2.21 Dyes
- •2.22 Intravitreal Injections
- •2.22.1 Injection Medications
- •2.23 Slow Release Preparations
- •2.24 Summary
- •References
- •3: Principles of Internal Tamponade
- •3.1 Gases
- •3.1.1 Principles
- •3.1.1.1 Properties
- •3.1.1.2 A Safe Method for Drawing Up Gas
- •3.1.2 Complications
- •3.1.2.1 Vision
- •3.1.2.2 Refraction
- •3.1.2.3 Cataract
- •3.1.2.5 Loss of the Gas Bubble
- •3.1.2.6 Gas in the Wrong Place
- •3.1.3 Important Postoperative Information
- •3.1.3.1 Flying or Travel to High Altitude
- •3.1.3.2 General Anaesthesia
- •3.2 Silicone Oil
- •3.2.1 Properties
- •3.2.3 Complications of Silicone Oil
- •3.2.3.1 Refractive Changes
- •3.2.3.2 Cataract
- •3.2.3.5 Cornea
- •3.2.3.6 Macular Toxicity
- •3.2.3.7 Oil in the Wrong Place
- •3.2.3.8 Emulsion
- •3.2.3.9 IOLs
- •3.2.4 Silicone Oil Removal
- •3.2.4.1 Alternative Methods
- •3.2.4.2 Retinal Redetachment Rates After Oil Removal
- •3.2.5 Heavy Silicone Oils
- •3.2.6 Heavy Liquids
- •3.2.7 ‘Light’ Heavy Liquids
- •3.3 Summary
- •References
- •4: Posterior Vitreous Detachment
- •4.1 Introduction
- •4.1.1 Symptoms
- •4.1.1.1 Floaters
- •4.1.1.2 Flashes
- •Introduction
- •Clinical Characteristics
- •4.1.2 Signs
- •4.1.2.1 Detection of PVD
- •4.1.2.2 Shafer’s Sign
- •4.1.2.3 Vitreous Haemorrhage
- •4.1.2.4 Ophthalmoscopy
- •4.1.3 Retinal Tears
- •4.1.3.1 U Tears
- •4.1.3.2 Atrophic Round Holes
- •4.1.3.3 Other Breaks
- •4.1.3.4 Progression to Retinal Detachment
- •4.1.4 Peripheral Retinal Degenerations
- •4.2 Summary
- •References
- •5: Vitreous Haemorrhage
- •5.1 Introduction
- •5.2 Aetiology
- •5.3 Natural History
- •5.4 Erythroclastic Glaucoma
- •5.5 Investigation
- •5.6 Ultrasound
- •5.7 Management
- •5.8 Surgery
- •5.9 Vitrectomy
- •5.10 Summary
- •References
- •6: Rhegmatogenous Retinal Detachment
- •6.1 Introduction
- •6.1.1 Tears with Posterior Vitreous Detachment
- •6.1.2 Breaks Without Posterior Vitreous Detachment
- •6.1.3 Natural History
- •6.1.3.1 Chronic RRD
- •6.1.3.2 Risk to the Other Eye
- •6.2 Clinical Features
- •6.2.1 Anterior Segment Signs
- •6.2.2 Signs in the Vitreous
- •6.2.3 Subretinal Fluid Accumulation
- •6.2.4 Retinal Break Patterns in RRD
- •6.2.5 Macula Off or On
- •6.3 Surgery
- •6.3.1 Flat Retinal Breaks
- •6.3.1.1 Retinopexy
- •6.3.1.2 Cryotherapy
- •6.3.1.3 Cryotherapy in the Clinic Setting
- •6.3.1.4 Laser
- •6.3.1.5 Laser in the Clinic Setting
- •6.3.2 Retinal Detachment
- •6.3.2.1 Principles
- •6.3.2.2 Break Closure
- •6.3.2.3 Relief of Traction
- •6.3.2.4 Alteration of Fluid Currents
- •6.3.2.5 Retinopexy
- •6.3.3 Pars Plana Vitrectomy
- •6.3.3.1 Introduction
- •6.3.3.2 Finding the Breaks
- •6.3.3.4 Draining Subretinal Fluid
- •6.3.3.5 When to Use Heavy Liquids
- •6.3.3.6 Removal of Heavy Liquid
- •6.3.3.7 Choice of Tamponade
- •6.3.3.8 Avoiding Retinal Folds
- •6.3.3.9 Inferior Breaks
- •6.3.3.10 Posterior Breaks
- •6.3.3.11 Multiple Breaks
- •6.3.3.12 Medial Opacities
- •6.3.3.13 Complications
- •6.3.3.14 Surgery for Eyes with No Breaks Found
- •6.3.3.15 Use of 360° Laser or Routine 360° Encirclage
- •6.3.3.16 Posturing
- •6.3.4.1 Operative Stages
- •6.3.4.2 Postoperative Care
- •6.3.4.3 Complications
- •6.3.4.4 Peroperative
- •6.3.4.5 Postoperative
- •6.3.5 Drainage Air Cryotherapy and Explant (DACE)
- •6.3.5.1 Subretinal Fluid (SRF) Drainage
- •6.3.5.2 Air Insertion
- •6.3.5.3 Complications
- •6.3.6 Pneumatic Retinopexy
- •6.3.6.1 Surgical Steps
- •6.3.6.2 Complications
- •6.4 Success Rates
- •6.5 Causes of Failure
- •6.6 Surgery for Redetachment
- •6.7 Secondary Macular Holes
- •6.8 Detachment with Choroidal Effusions
- •6.9 Removal of Explant
- •6.9.1 Diplopia
- •6.9.2 Erosion Through Conjunctiva
- •6.9.3 Infection
- •6.9.4 Cosmesis
- •6.9.5 Irritation
- •6.9.6 Surgery for Removal of the Explant
- •6.10 Summary
- •References
- •7.2 Atrophic Hole RRD with Attached Vitreous
- •7.3 Pseudophakic RRD
- •7.4 Aphakic RRD
- •7.5 Retinal Dialysis
- •7.5.1 Clinical Features
- •7.5.2 Surgery for Retinal Dialysis
- •7.5.2.1 Search
- •7.5.2.2 Cryotherapy
- •7.5.2.3 Marking the Break
- •7.5.2.4 Plombage
- •7.5.2.5 Checking the Indent
- •7.5.3 Complications
- •7.5.4 Giant Retinal Dialysis
- •7.5.5 Dialysis and PVR
- •7.5.6 Par Ciliaris Tear
- •7.6 Giant Retinal Tear
- •7.6.1 Clinical Features
- •7.6.2 Stickler’s Syndrome
- •7.6.3 Surgery for Giant Retinal Tear
- •7.6.3.1 Heavy Liquids
- •7.6.3.2 Retinopexy
- •7.6.3.3 Trans-scleral Illumination Technique
- •7.6.3.4 Silicone Oil Insertion
- •7.6.3.5 Choice of Endotamponade
- •7.6.3.6 Success Rates
- •7.6.3.7 Removal of the Silicone Oil
- •7.6.3.8 The Other Eye
- •7.7 Retinal Detachment in High Myopes
- •7.7.1 Clinical Features
- •7.7.2 Surgery
- •7.8.1 Clinical Features
- •7.8.1.1 Infantile Retinoschisis
- •7.8.1.2 Senile Retinoschisis
- •7.8.1.4 Retinal Detachment in Retinoschisis
- •7.8.2 Surgery
- •7.9 Juvenile Retinal Detachment
- •7.10 Atopic Dermatitis
- •7.11 Refractive Surgery
- •7.12 Congenital Cataract
- •7.13 Others
- •7.14 Summary
- •References
- •8: Proliferative Vitreoretinopathy
- •8.1 Introduction
- •8.2 Pathogenesis
- •8.3 Clinical Features
- •8.3.1 Introduction
- •8.3.2 Grading
- •8.3.3 Risk of PVR
- •8.4 Surgery
- •8.4.1 Mild PVR
- •8.4.2 Moderate PVR
- •8.4.3 Severe PVR
- •8.4.3.1 The Relieving Retinectomy
- •8.4.4 Radial Retinotomy
- •8.4.5 Silicone Oil Injection
- •8.4.6 Applying Laser
- •8.4.7 ROSO Plus
- •8.4.8 Very Severe PVR
- •8.4.9 Choice of Endotamponade
- •8.4.9.1 Silicone Oil or Perfluoropropane Gas
- •8.4.9.2 Heavy Oils
- •8.4.10 Removal of Subretinal Bands
- •8.4.11 Adjunctive Therapies
- •8.4.12 Success Rates
- •8.4.13 Postoperative Complications
- •8.5 Summary
- •References
- •9: Macular Hole
- •9.1 Introduction
- •9.2 Idiopathic Macular Hole
- •9.2.1 Clinical Features
- •9.2.1.1 Introduction
- •9.2.1.2 Watzke–Allen Test
- •9.2.1.3 Grading
- •9.2.1.4 Natural History
- •9.2.1.5 Optical Coherence Tomography
- •9.2.2 Secondary Macular Holes
- •9.2.3 Lamellar and Partial Thickness Holes
- •9.2.4 Surgery
- •9.2.4.1 Introduction
- •9.2.4.2 Surgery
- •9.2.4.3 Peeling the Posterior Hyaloid Membrane
- •9.2.4.4 ILM Peel and Other Adjunctive Therapies
- •9.2.4.5 Choice of Tamponade
- •9.2.4.6 Postoperative Posturing of the Patient
- •9.2.4.9 Visual Field Loss
- •9.2.5 Success Rates
- •9.2.6 Reoperation
- •9.3 Microplasmin
- •9.4 Summary
- •References
- •10.1 Clinical Features
- •10.1.1 Other Conditions
- •10.1.2 Secondary Macular Pucker
- •10.2 Surgery
- •10.3 Success Rates
- •10.5 Membrane Recurrence
- •10.6 Summary
- •References
- •11: Choroidal Neovascular Membrane
- •11.1 Age-Related Macular Degeneration
- •11.1.1 Clinical Features
- •11.1.2 Vitreous Haemorrhage and CNV
- •11.1.3 Pneumatic Displacement of Subretinal Haemorrhage
- •11.1.4 Surgery for Failed Anti-VEGF Therapy
- •11.1.4.1 Introduction
- •11.1.4.2 360° Macular Translocation
- •11.1.6 Success Rates
- •11.2 Choroidal Neovascular Membrane Not from ARMD
- •11.2.1 Introduction
- •11.2.2 Surgery
- •11.3 Summary
- •References
- •12: Diabetic Retinopathy
- •12.1 Introduction
- •12.2 Diabetic Retinopathy
- •12.2.1 Introduction
- •12.2.1.1 Diabetic Retinopathy Grading
- •12.2.2 Diabetic Vitreous Haemorrhage
- •12.2.3 Progression to Vitreous Haemorrhage and Tractional Retinal Detachment
- •12.2.3.1 Clinical Features
- •12.2.3.2 Surgery
- •12.2.4 Diabetic Retinal Detachment
- •12.2.4.1 Clinical Features
- •12.2.4.2 Surgery
- •12.2.4.3 Tractional Retinal Detachment
- •12.2.4.4 Peroperative Panretinal Photocoagulation
- •12.2.4.6 Bimanual Surgery
- •12.2.4.7 Dealing with Bleeding Vessels
- •12.2.4.8 Iatrogenic Breaks
- •12.2.4.9 Silicone Oil
- •12.2.4.10 Combined TRD and RRD
- •12.2.5 Postoperative Complications
- •12.2.5.1 Vitreous Haemorrhage
- •12.2.5.2 Rhegmatogenous Retinal Detachment
- •12.2.5.3 Iris Neovascularisation
- •12.2.5.4 Phthisis Bulbi
- •12.2.5.5 Maculopathy
- •12.2.5.6 Survival After Surgery
- •12.2.6 Success Rates
- •12.2.7 Diabetic Maculopathy
- •References
- •13: Other Vascular Disorders
- •13.1 Introduction
- •13.2 Retinal Vein Occlusion
- •13.2.1 Chorioretinal Anastomosis
- •13.2.2 Arteriovenous Decompression
- •13.2.3 Radial Optic Neurotomy
- •13.2.4 Intravitreal Steroid and Anti-VEGF Agents
- •13.2.5 Tissue Plasminogen Activator
- •13.3 Sickle-Cell Disease
- •13.3.1 Introduction
- •13.3.2 Types of Sickle-Cell Disease
- •13.3.3 Systemic Investigation
- •13.3.4 Inheritance and Race
- •13.3.5 Systemic Manifestations
- •13.3.6 Ophthalmic Presentation
- •13.3.7 Laser Therapy
- •13.3.8 Surgery
- •13.3.9 Visual Outcome
- •13.3.10 Screening
- •13.3.11 Survival
- •13.4 Retinal Vasculitis
- •13.5 Central Retinal Artery Occlusion
- •13.6 Summary
- •References
- •14: Trauma
- •14.1 Introduction
- •14.3 Contusion Injuries
- •14.3.1 Clinical Presentation
- •14.3.2 Types of Retinal Break
- •14.3.2.1 Dialysis
- •14.3.2.2 Pars Ciliaris Tears
- •14.3.2.3 Ragged Tear in Commotio Retinae
- •14.3.2.4 Giant Retinal Tears
- •14.3.3 Surgery
- •14.3.4 Visual Outcome
- •14.4 Rupture
- •14.4.1 Clinical Presentation
- •14.4.2 Surgery
- •14.4.3 Visual Outcome
- •14.5 Penetrating Injury
- •14.5.1 Clinical Presentation
- •14.5.1.1 Endophthalmitis
- •14.5.1.2 Retinal Detachment
- •14.5.2 Surgery
- •14.5.3 Visual Outcome
- •14.6 Trauma Scores
- •14.7 Intraocular Foreign Bodies
- •14.7.1 Clinical Presentation
- •14.7.1.1 Diagnostic Imaging
- •14.7.2 IOFB Materials
- •14.7.3 Surgery
- •14.7.4 The Primary Procedure
- •14.7.5 PPV: The Anterior Segment
- •14.7.5.1 The Lens
- •14.7.6 PPV: The Posterior Segment
- •14.7.7 The Magnet
- •14.7.8 Visual Outcome
- •14.7.9 Siderosis
- •14.8 Perforating Injury
- •14.9 Sympathetic Ophthalmia
- •14.10 Proliferative Vitreoretinopathy
- •14.11 Phthisis Bulbi
- •14.12 When Not to Operate
- •14.12.1 At Presentation
- •14.12.2 Postoperatively
- •14.13 Summary
- •References
- •15.1 Introduction
- •15.2 Dropped Nucleus
- •15.2.1 Clinical Features
- •15.2.2 Surgery
- •15.2.2.1 Primary Management
- •15.2.2.2 Vitrectomy Surgery
- •15.2.2.4 Success Rates
- •15.3 Intraocular Lens Dislocations
- •15.3.1 Clinical Presentation
- •15.3.2 Surgery
- •15.3.2.1 Removal of the IOL
- •15.4 Surgical Options for the Aphakic Eye
- •15.4.1 McCannell Sutured IOL
- •15.4.2 Iris-Clip IOL
- •15.4.3 Haptic Capture Method
- •15.4.4 Anterior Chamber IOL
- •15.4.5 Sutured Posterior Chamber IOLs
- •15.4.6 The Aphakic and Aniridic Eye
- •15.5 Postoperative Endophthalmitis
- •15.5.1 Clinical Features
- •15.5.2 Surgery
- •15.5.2.1 Vitreous Tap
- •15.5.2.2 Vitreous Biopsy
- •15.5.3 Infective Organisms
- •15.5.4 Antibiotics
- •15.5.5 The Role of Vitrectomy
- •15.5.6 Success Rates
- •15.6 Chronic Postoperative Endophthalmitis
- •15.7 Needlestick Injury
- •15.7.1 Clinical Features
- •15.7.2 Surgery
- •15.8 Intraocular Haemorrhage
- •15.9 Retinal Detachment
- •15.10 Chronic Uveitis
- •15.11 Postoperative Cystoid Macular Oedema
- •15.12 Postoperative Vitreomacular Traction
- •15.13 Postoperative Choroidal Effusion
- •15.13.1 External Drainage
- •15.14 Summary
- •References
- •16: Uveitis and Allied Disorders
- •16.1 Introduction
- •16.2 Non-infectious Uveitis of the Posterior Segment
- •16.2.2 Retinal Detachment
- •16.2.3 Cystoid Macular Oedema
- •16.2.4 Hypotony
- •16.2.5 The Vitreous Biopsy
- •16.2.6 Sampling at the Beginning of a PPV
- •16.2.6.1 Special Situations
- •16.3 Acute Retinal Necrosis
- •16.3.1 Clinical Features
- •16.3.2 Surgery
- •16.3.2.1 For Diagnosis
- •16.3.2.2 For Treatment
- •16.3.3 Visual Outcome
- •16.4 Cytomegalovirus Retinitis
- •16.4.1 Clinical Features
- •16.4.2 Surgery
- •16.4.2.1 For Diagnosis
- •16.4.2.2 For Treatment
- •16.4.3 Visual Outcome
- •16.5 Fungal Endophthalmitis
- •16.5.1 Clinical Features
- •16.5.2 Surgery
- •16.5.2.1 For Diagnosis
- •16.5.2.2 For Treatment
- •16.5.3 Visual Outcome
- •16.6 Other Infections
- •16.6.1 Clinical Features
- •16.6.2 Surgery
- •16.6.2.1 For Diagnosis
- •16.6.2.2 Chorioretinal Biopsy
- •16.6.2.3 For Treatment
- •16.6.3 Visual Outcome and Survival
- •16.7 Paraneoplastic Retinopathy
- •16.8 Summary
- •References
- •17: Miscellaneous Conditions
- •17.1 Vitrectomy for Vitreous Opacities
- •17.2 Vitreous Anomalies
- •17.2.1 Persistent Hyperplastic Primary Vitreous
- •17.2.2 Asteroid Hyalosis
- •17.2.3 Amyloidosis
- •17.3 Retinal Haemangioma and Telangiectasia
- •17.4 Optic Disc Anomalies
- •17.4.1 Optic Disc Pits and Optic Disc Coloboma
- •17.4.2 Morning Glory Syndrome
- •17.5 Retinochoroidal Coloboma
- •17.6 Marfan’s Syndrome
- •17.7 Retinopathy of Prematurity
- •17.8 Uveal Effusion Syndrome
- •17.8.1 Clinical Features
- •17.8.2 Surgery
- •17.9 Terson’s Syndrome
- •17.10 Disseminated Intravascular Coagulation
- •17.11 Retinal Prosthesis
- •17.12 Summary
- •References
- •Glossary of Abbreviations
- •Others in Database
- •Appendices
- •Useful Formulae and Rules
- •Cryotherapy
- •Fluids (i.e. Both Gases and Liquids)
- •Gases
- •Liquids
- •Ultrasound
- •Diffusion and Viscosity
- •Visual Acuity
- •Diffusion
- •Fick’s Law
- •Stokes-Einstein
- •Darcy’s Law
- •Starling’s Law
- •Index
4.1 Introduction |
|
|
|
|
|
|
93 |
|
|
|
|
|
|
|
|
Table 4.2 Different presentations of flashes |
|
|
|
|
|
|
|
Flashes |
|
|
|
|
|
|
|
Diagnosis |
Duration |
Colour |
Location |
Shape |
Stimulus |
Other symptoms |
Flickering |
PVD |
Seconds or less |
White |
Temporal |
Crescentic |
Eye movements |
Floaters |
No |
|
|
|
periphery |
vertical |
|
|
|
Migraine |
20–30 min |
Not |
Paracentral |
Arcuate |
Stress, food |
Scotoma |
Yes |
|
|
typically |
|
Zigzag |
|
headache nausea |
|
Occipital ischemia |
Minutes |
Nil |
Central |
Petaloid |
Neck move- |
|
Yes |
|
|
|
|
|
ments exertion |
|
|
Cystoid macular oedema |
Constant |
Variable |
Central |
Pinpricks |
Nil |
Poor vision |
Yes |
Outer retinal or RPE |
Minutes |
Blue |
Paracentral |
Blobs |
Nil |
Scotoma |
No |
abnormality |
|
Purple |
|
Spirals |
|
|
|
Retinal detachment |
Seconds |
Golden |
Central/paracentral |
Comet oblique |
Eye movements |
Visual field loss |
No |
|
|
|
|
horizontal |
|
|
|
ring separates, the symptoms change to floaters and lightning flashes. Typically, the lightning flashes of PVD are vertical, temporally placed and instantaneous flashes. If the flashes in a patient with PVD are oblique or horizontally orientated, not in the temporal visual field or not typical instantaneous flashes, the patient is more likely to have a PVD with a retinal tear or rhegmatogenous retinal detachment (Goodfellow et al. 2009).
These visual phenomena should be discriminated from the flashes that occur with other disorders, such as the zigzag lights of migraine, flickering stars associated with occipital ischaemia and the rare coloured lights of the acute zonal outer occult retinopathy (AZOOR) syndromes. Mostly, this photopsia is centrally placed in the visual field and therefore can be easily discriminated. Slower more mid-peripheral flashes are produced by the leading edge of some retinal detachments often shaped like a comet’s tail.
Patients who experience symptoms during posterior vitreous separation have a 10 % risk of developing a retinal tear (van Overdam et al. 2001; Sharma et al. 1999; Hikichi and Trempe 1994). Flashes from PVD usually subside in a few months, whilst floaters get less but may not disappear entirely (Serpetopoulos 1997). The floaters lessen as the opacities on the posterior surface of the vitreous sink lower in the eye but also because they move anteriorly and are less in focus than when they were nearer the inner surface of the retina. Severe floaters can be bothersome, and in a few patients, PPV is required to clear the vision. Rarely flashes will persist for years more often associated with vitreous attached young myope RRD (i.e. flashes associated with RRD rather than PVD) and very rarely after PVD. Occasionally, patients will have flashes after PPV.
4.1.2Signs
4.1.2.1 Detection of PVD
A posterior vitreous detachment can be diagnosed by examining the eye with a 90-dioptre lens. Definitively, if a
Fig. 4.10 In an eye with forward displacement of a PVD, the posterior hyaloid membrane can be seen in the anterior vitreous cavity
Weiss ring is present, then a PVD has occurred. Sometimes this is not obvious, but it is possible to see the posterior hyaloid membrane. This is more subjective, but it can be reassuring to observe the space behind the membrane; if this is optically clear, it suggests that there is no vitreous gel at this location. A partial posterior vitreous detachment is a diagnosis that should be made only with care. It can be extremely difficult to determine whether there are remaining vitreous attachments. Likely residual attachments are at the optic disc, chorioretinal scars and epiretinal membranes at the macula and neovascular tissue. Usually, a posterior vitreous detachment occurs completely, soon after the onset of symptoms probably in a few hours. There remain a few patients in whom the posterior vitreous detachment progresses over a few weeks as evidenced by the formation of new retinal breaks in the first 6 weeks after onset of symptoms in 1.8–3.4 % (Hollands et al. 2009).
4.1.2.2 Shafer’s Sign
In most patients with tears, retinal pigment epithelial cells released through the tear will be visible in the anterior vitreous (Shafer’s sign). This is highly predictive of a retinal tear
94 |
4 Posterior Vitreous Detachment |
|
|
Fig. 4.11 Pigment granules in the vitreous are good indicators of the presence of a retinal tear from PVD
(approximately 90 %) (Tanner et al. 2000; Dayan et al. 1996; Byer 1994; Brod et al. 1991; Sharma et al. 1999). In symptomatic PVD, 10 % of patients will develop retinal tears. Most tears are present when the patient presents; however, 10 % of tears are be detected at 6 weeks from onset of symptoms (constituting theoretically 1 % of all cases with symptomatic PVD) (Richardson et al. 1999; Dayan et al. 1996). Breaks found in asymptomatic eyes are less likely to lead to retinal detachment (Byer 1998).
The pigment granules in Shafer’s sign are relatively large (diameter of 30–50 mm), pigmented and are seen in the anterior vitreous especially often inferiorly. The patient, therefore, should be examined during eye movements, allowing inferior vitreous to present itself for examination in the pupil. Only one granule is required to make the diagnosis of Shafer’s sign and indicate the risk of a retinal tear.
4.1.2.3 Vitreous Haemorrhage
Red blood cells (RBCs) which are smaller, 6–8 mm, may also be seen and should also raise suspicion of pathology although this is less indicative than pigment granules with 50 % of patients with RBCs in vitreous having retinal tears. Sometimes the haemorrhage is severe, preventing visualisation of all or part of the retina. This should be investigated by ultrasound, and a PPV is performed urgently to allow detection of breaks. In some patients, a superior break might be seen, but the inferior retina might be obscured by inferior vitreous haemorrhage. The surgeon may be tempted to laser the superior break and observe; however, because of the chance of multiple breaks (approximately 50–60 %) and the suspected increased risk of PVR in the presence of haemorrhage, it is safer to proceed to PPV allowing examination of the inferior retina (also see Chap. 5).
Fig. 4.12 Erythrocytes in the vitreous indicate a 50 % chance of finding and retinal break in an acute PVD
4.1.2.4 Ophthalmoscopy
Note: The patient requires 360° examination of the retina with indirect ophthalmoscopy and indentation of the far periphery.
This aids identification of breaks both by introducing peripheral retina into the view but also allowing a dynamic observation of a break. The break can be opened up and more clearly seen by movement of the retina. Moving the choroid under the break changes the colour of the choroid seen through the orifice of the break discriminating a break from retinal haemorrhage or pigmentation which remains the same colour despite indentation. If a patient presents early with PVD, it is worth re-examining the retina at 6 weeks after symptoms occur because 1.8–3.4 % will have tears seen at the second examination that were not seen at the first (Coffee et al. 2007). If patients have vitreous haemorrhage, retinal haemorrhage or develop new symptoms, they may be more likely to have breaks seen at the second examination.
Note: If a patient presents early with PVD symptoms of a few days, another examination at 1–2 weeks is useful.
|
Odds ratio for detection |
|
|
of a retinal break |
95 % confidence |
|
(Hollands et al. 2009) |
interval |
Subjective vision |
5.0 |
3.1–8.1 |
reduction |
|
|
Vitreous haemorrhage |
10 |
5.1–20 |
Absence of vitreous |
0.23 |
0.12–0.43 |
pigmentation |
|
|
Other Signs
PVD may induce optic disc haemorrhages (causing subtle visual field loss) (Katz and Hoyt 1995; Roberts and
