- •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
72 |
3 Principles of Internal Tamponade |
|
|
Table 3.4 Silicone oil complications
Silicone oil complications |
Duration from surgery |
|
|
|
Complication |
0–3 months |
3–12 months |
1–2 years |
2–10 years |
Overfill glaucoma |
Yes |
No |
No |
No |
Pupil block glaucoma in aphake |
Yes |
Occasional if peripheral iridectomy closes |
||
Open-angle glaucoma |
Unlikely |
Occasional |
Common |
Common |
Cataract |
Unlikely |
Occasional |
Common |
Common |
Oil-induced macular visual loss |
Occasional |
Occasional |
Unlikely |
Unlikely |
Band keratopathy |
No |
No |
Unlikely |
More common |
Emulsion of oil |
Unlikely |
Occasional |
Common |
Common |
In some eyes, the defect in the zonule allows a bubble of oil to re-enter the eye during these manipulations (seen first as a bulge in the iris and then the bubble floats into the anterior chamber), but this is usually a small bubble which can be removed by repeating step one above. If the lens is dislocated or very unstable (e.g. in a patient with trauma or a complicated cataract extraction) and oil keeps coming through into the anterior chamber, you may need to remove the lens and capsule leaving the eye aphakic (remember to perform an inferior peripheral iridectomy).
There seems to be a threshold size of bubble in the AC which can cause pupil block; anything less than 2 mm diameter is safe. However, it is not recommended to leave oil in the AC; therefore, by using the techniques above, remove any AC oil at the end of the operation.
Note: When filling the eye with oil, think ‘volume rather than pressure’. Once the oil is near a maximal fill in the vitreous cavity, a tiny increase in volume causes a large increase in IOP because you are inserting a noncompressible liquid into a relatively stiff-walled container. To maximise the fill, the key is to remove the residual aqueous layer and SRF. The IOP can be kept at a low level (7 mmHg) without detriment to the fill. The fill is determined by the volumetric removal of the aqueous component and its replacement with a volume of oil and not by increased pressure in the oil bubble (and therefore the aqueous component) which in the rigid container does not increase the volume of the oil.
3.2.3Complications of Silicone Oil
Fig. 3.18 A CT scan of an eye with silicone oil in situ and a silicone encircling band. The curved inferior edge of the oil is apparent demonstrating the lack of contact with the retina in this case posteriorly (patient is face up)
These are numerous.
3.2.3.1 Refractive Changes
•The oil has a higher refractive index than vitreous or water and therefore induces refractive errors primarily determined on whether the oil surface anteriorly is concave or convex. A concave profile occurs in phakic eyes; radius of the posterior lens is −8.10 mm, effectively reversing the refraction at the posterior lens because the lens and oil have refractive indices of 1.37 for the lens and 1.4 for oil, compared with 1.33 for water/vitreous.
Fig. 3.19 In the face up position, the oil can be seen with little contact with the retina in this section
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This induces a need for a hypermetropic correction of approximately +5D; therefore, in a high myope, the myopia is reduced. In pseudophakic eyes, the IOL usually has a flatter profile to the posterior lens surface and
Oil
Fig. 3.20 Silicone oil in an aphakic eye produces a convex lens at the point of the pupil, thereby producing a myopic shift. In aphakic eyes, the degree of hypermetropia is reduced by silicone oil insertion
Emetropia
Oil
Crystalline lens
has a refractive index as high as 1.55. When oil is inserted, a hypermetropic shift is again induced. In both, the total refraction of the eye is reduced to approximately +50D. In an aphakic eye, the anterior surface is convex inducing a myopic shift in refraction of approximately +5D, thereby reducing the aphakic correction from +10D to +5D again giving a total refraction of the eye of about +50D.
•Note in a high myope the hypermetropic shift may reduce the degree of myopia. The opposite occurs in aphakic eyes where the oil bulges through the pupil (reducing the aphakic correction by approximately +5D).
3.2.3.2 Cataract
•Silicone is associated with a formation of nuclear sclerotic cataract, which may occur in complex retinal detachments especially with PVR, but is exacerbated by presence of the oil.
3.2.3.3 Capsule Opacification
•A posterior capsule in a pseudophake will thicken severely with oil with time.
Oil
Aphakia
Oil
IOL
Fig. 3.21 The whole refractive power of the eye is reduced when oil is inserted; therefore, the patient needs a +D spectacle lens to compensate. This is because the refractive power of the posterior surface of the crystalline lens is neutralised by the oil, that is, the difference in refractive
index between the oil and the lens is much less than water (vitreous) and the lens. The effect on the refraction of the eye is similar in an eye with aphakia, pseudophakia or with a crystalline lens
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3.2.3.4 IOP
•The trabecular meshwork can be filled with silicone oil droplets causing open-angle glaucoma in at least 40 % (Honavar et al. 1999) which is difficult to treat with 28 % remaining refractory to treatment.
Fig. 3.22 A patient has oil in situ and has low-tension glaucoma. This has exacerbated the glaucoma and caused a severe optic disc cup from additional silicone oil and disc glaucoma
•Angle closure glaucoma in aphakic eyes is produced if a peripheral iridectomy closes (seen in up to 33 %) and the oil bulges through the pupil (Madreperla and McCuen 1995). This can be diagnosed in an eye with a deep anterior chamber, with a clear cornea but a raised intraocular pressure. A sheen may be seen in the iris crypts suggesting oil in the anterior chamber; a cross-sectional slit beam reveals that no cells or flare are present in the anterior chamber and there are no visible convection currents suggesting normal aqueous. Reopening of a peripheral iridectomy will re-establish fluid flow pushing the oil back into the posterior chamber reducing the pressure. YAG peripheral iridectomies tend to close over again in a few weeks; therefore, a surgical iridectomy is preferred. Even the latter may close in 5–33 % of eyes with silicone oil (Madreperla and McCuen 1995; Elliott et al. 1990).
•In phakic or pseudophakic eyes, oil which has dislocated into the anterior chamber, usually peroperatively, can cause an unusual pupil block glaucoma in which the lens is pushed backwards and the iris is pushed anteriorly (Jackson et al. 2001). This causes intermittent angle closure glaucoma which can be difficult to diagnose in the postoperative period. Peripheral iridectomies are usually only temporally effective, and removal of silicone oil is required.
Fig. 3.23 This patient has thinning of the retinal nerve fibre layer from oil-induced glaucoma
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If the oil is required for permanent tamponade, the lens capsule complex may need to be removed and an inferior peripheral iridectomy performed in the aphakic eye thus created. Oil presenting into the anterior chamber peroperatively should be evacuated with viscoelastic (see earlier in the chapter, silicone oil in the anterior chamber).
•In some circumstances, there is a deep anterior chamber, and the oil is behind the pupil, but there is still raised intraocular pressure. This may indicate an overfill situation. In an aphakic eye, oil can be removed via a paracentesis reducing the volume of silicone in the eye. In the phakic eye, oil will need to be removed through a sclerotomy. The inexperienced surgeon should avoid the temptation to maximise the fill of oil by leaving the eye ‘hard’ (high IOP) at the end of the operation. In fact, because of the physical properties of a sphere filled with a liquid, increasing the IOP does not make a significant change in the volume of the filling liquid in the cavity; see Appendix.
3.2.3.5 Cornea
•The oil is associated with the occurrence in some patients of band keratopathy. Some of these eyes are already extensively damaged. The keratopathy may be partly due to phthisis of the eye, which has been prevented by the oil, rather than by contact of the oil on the cornea itself.
3.2.3.6 Macular Toxicity
•Toxicity to the retina in its severest form may result in occasional patients suffering loss of central vision either with the oil in situ or around the time of oil removal (Herbert et al. 2005a, b, 2006; Newsom et al. 2005). For the latter, always avoid direct illumination of the macula during oil removal as the macula seems to be prone to light toxicity in oil-filled eyes. Unfortunately, the loss of vision is permanent often down to 20/200. There is associated relative central scotoma and reduction in colour sensation in the scotoma. OCT images have not shown a detectable abnormality in the retina so far, and electrophysiology has been inconclusive, showing defects in retinal and optic nerve function.
•Pathologically, the oil impregnates all the areas of the eye with characteristic foamy macrophages. Therefore, it has some mild effect on reducing visual acuity through effects on the retina.
3.2.3.7 Oil in the Wrong Place
•There are complications from oil in the wrong place such as subretinal, suprachoroidal or subconjunctival.
•Subretinal oil is very likely to be associated with a total retinal detachment. This may happen if the infusion cannula tip moves into the subretinal space during
Fig. 3.24 To create an inferior peripheral iridectomy (PI) in an aphake with oil in situ, use the cutter on ‘aspirate only’ to engage the iris, then on low cut rate (200 cuts/min), remove a portion of the peripheral iris. Make sure there is no lens capsule or vitreous behind the PI
Fig. 3.25 Small bubbles of oil in the AC do not usually cause pupil block. The spherical shape of the bubble minimises the area of oil in contact with the corneal endothelium. Corneal decompensation is rare. The oil can have refractive effects on the vision
infusion of the oil. If the eye goes hypotonous during surgery, the tip may angle under the retina, especially if the anterior retina is elevated because of anterior contraction in proliferative vitreoretinopathy or because of retinal detachment into the ciliary body in preoperative hypotony. Once noticed, the oil should be evacuated, but this will usually require a retinectomy. The retinectomy should be large enough to allow the oil to pass through the hole (at least 2 clock hours) overcoming its
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Fig. 3.26 A large bubble of oil in the AC may cause pupil block which is only temporarily relieved by peripheral iridectomy and usually requires oil removal from the AC and if possible from the posterior segment
Fig. 3.27 Oil has entered the anterior chamber despite a patent peripheral iridectomy because this eye has become hypotonous and is no longer producing enough aqueous to keep the anterior chamber filled
surface tension. Postoperative movement of oil into the subretinal space is seen in the presence of large retinal breaks (or breaks that have become larger postoperatively because of traction) with continued contraction of epiretinal membranes usually PVR, for example, severe tractional and rhegmatogenous retinal detachment in diabetes.
•Suprachoroidal oil is a very rare occurrence and is again caused by problems with the infusion cannula moving
Fig. 3.28 Oil has entered the eye through the zonules of this phakic eye and has pushed the iris forwards and created pupil block glaucoma with a deep anterior chamber
Oil
Fig. 3.29 Silicone oil trapped in the anterior chamber can cause forward projection of the pupil and iris and backprojection of the intraocular lens, causing pupil block glaucoma
as above but into the suprachoroidal space. A retinectomy and choroidectomy will be needed to evacuate the oil. The incisions should be anterior to allow the oil to float out. Alternatively cut down on the sclera to access the suprachoroidal space.
•Subconjunctival oil is extremely difficult to remove because it infiltrates the Tenon’s layer with multiple small bubbles causing inflammation. It is caused by poor closure of a sclerotomy and possibly raised IOP. This should be seen very rarely.
