- •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
40 |
2 Introduction to Vitreoretinal Surgery |
|
|
Fig. 2.34 This patient had a ßoater after a PPV for RRD. There was a Þlament from a gauze swab (arrow) in the vitreous cavity which was washed out by repeat PPV. It is important that materials which can produce Þlaments are not used near vitrectomy surgery in case Þlaments enter the eye as in this case
rotic opacity similar to age-related cataract appears. In those under 50 years, the nuclear sclerosis is white. Risk of postoperative cataract is:
1. Low if the patient is less than 50 years old. 2. Approximately 30 %, when no gas is used.
3. 17Ð37 % when the patient is diabetic (Schachat et al. 1983). Increased pO2 in the vitreous cavity has been implicated in cataract formation post PPV (Holekamp et al. 2005); lower pO2 in diabetes may explain the reduced risk of cataract after PPV in diabetes (Holekamp et al. 2006).
4. 80 % if the patient is more than 50 years old or gas or silicone oil is used.
5. 70 % of PPV for RRD get cataract.
6. 83 % of macular holes at 3 years have had IOL implantation.
The mean time to phacoemulsiÞcation operation after PPV in a Californian practice was 20 months (Grusha et al. 1998). In one study of 301 eyes using 4 grades of cataract, these were the progression rates (Thompson 2004):
<50 years |
0.13 grades/year |
>50 years |
0.7Ð0.9 grades/year |
Intraocular gas |
0.8 grades/year |
No gas bubbles |
0.5 grades/year |
insertion, the syringe may disconnect from the three-way tap (a common problem as silicone oil is often supplied in glass syringes which have ßimsy connection systems); see the section on silicone oil in Chap. 3.
Causes of peroperative hypotony
1.Blocked infusion cannula
2.Heavy liquid in the cannula
3.Faulty cassette
4.Faulty or wet air Þlter during air infusion
5. Water in the air line from incorrect rotation of the threeway tap
6.Faulty three-way tap
7.Leaking sclerotomies
8.Disconnection of an oil infusion syringe
9.Sclerotomies over draining
2.13Postoperative Complications
2.13.1 Cataract
Cataract formation occurs in almost all patients over the age of 50 years but is less common under this age and in diabetic patients with retinopathy. Cataract progression in the Þrst 6 months after surgery is likely if there is pre-existing cataract. Otherwise, the time taken to develop cataract may vary. In patients over 50 years of age, a typical yellow nuclear scle-
Gas cataracts are feathery posterior subcapsular lens opacities which are present in some patients when the gas bubble is present. Although these spontaneously resolve once the gas absorbs, they are associated with early onset of nuclear cataract.
Posterior subcapsular cataract occurs if the lens has been touched during surgery.
2.13.2 Endophthalmitis
Endophthalmitis is reported as low as 0.011Ð0.07 % (Eifrig et al. 2004; Cohen et al. 1995; Wykoff et al. 2010) in single centre studies but is increased when Medicare insurance forms are examined 0.3Ð0.4 % (Stein et al. 2009) and appears to involve the usual organisms (see Chap. 12). Early reports of small gauge surgery have reported an increased risk of endophthalmitis, but this has not been seen in later studies.
2.13.3 Corneal Changes
Corneal changes are reported in 27 % of eyes with tamponade of either oil or gas in PVR eyes (Abrams et al. 1995). If ßuid is allowed to ßow freely during vitrectomy, corneal changes similar to gutatta can be seen months after the surgery.
2.13 Postoperative Complications |
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Fig. 2.35 Corneal endothelial changes can be seen after PPV. These appear to be more common if high ßow rates of the infusion are used in PPV. Now that ßow rates are less because of self-sealing wounds or small gauge vitrectomy, corneal changes are less common
2.13.4 Choroidal Haemorrhage
Choroidal haemorrhage occurs in up to 1 % overall but is usually limited in area and associated with other manoeuvres such as external plombage (Narendran and Williamson 2003). Two types may be seen, those noticed peroperatively and those only seen postoperatively on the Þrst day. Retrospective studies report lower incidences at 0.1Ð0.17 % but may be underreporting small bleeds (Tabandeh et al. 1999; Sharma et al. 1997; Ghoraba and Zayed 2001), and Medicare forms show 0.5 % (Stein et al. 2009). IdentiÞed risk factors are myopia, pseudophakia or aphakia, rhegmatogenous retinal detachment, application of a buckle, previous surgery and cryotherapy (Figure 2.36). So far, warfarin therapy has not been associated with haemorrhagic complications from PPV and can be continued (Dayani and Grand 2006; Chandra et al. 2011). Cases of haemorrhage have been reported with combined antiplatelet agents, for example, clopidogrel (Herbert et al. 2006), but a cohort study has not shown increased risk with these agents (Mason et al. 2010).
2.13.5 Raised Intraocular Pressure
Raised IOP is relatively common in the Þrst few weeks after PPV (approximately 25 % of patients) occurring from a steroid response to postoperative drops, from intraocular gas expansion and rarely from malignant glaucoma. In the treatment of the last, make sure that there is an open channel between the posterior segment and the anterior segment to allow ßuid ßow. This requires removal of anterior vitreous on any other tissue (iris or lens capsule) which might occlude ßow of aqueous. It is usual to render the eye pseudophakic
Fig. 2.36 The presence of hyphaema on day one postoperatively suggests a severe posterior segment bleed either intravitreal or suprachoroidal. The patient must be monitored carefully in the postoperative period for elevation of the IOP and repeated ultrasounds performed to detect any RRD. Intervene early if RRD occurs as there is a high chance of PVR
Fig. 2.37 This chroidal haemorrhage is so severe that it has pushed the choroid and retina up behind the lens
and to remove the capsule and anterior vitreous behind a peripheral iridectomy.
A particular danger is raised IOP from the wrong gas mix which can cause central retinal artery occlusion; see Chap. 3.
2.13.6 Retinal Breaks and RRD
Inadequate clearance of vitreous from around sclerotomies and careless insertion of instruments can result in retinal breaks just posterior to the sclerotomies, known as entry
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2 Introduction to Vitreoretinal Surgery |
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Fig. 2.38 This traumatised eye developed aqueous misdirection and raised IOP with shallowing of the anterior chamber after vitrectomy. A capsulotomy at the edge of the IOL (arrow) allowed the aqueous to ßow
into the anterior chamber with a drop in the IOP and deepening of the anterior chamber
site breaks. These may develop in the postoperative period as the vitreous contracts into the sclerotomy pulling the retina and causing break formation. Entry site breaks have been described in approximately 3 % with aetiology of penetrating trauma increasing the incidence (Al-Harthi et al. 2005).
Other iatrogenic retinal breaks can appear from direct trauma from instruments scraping the retina, the cutter incising retina, peeling of the posterior hyaloid membrane or traction on the vitreous base. It is important not to miss peroperative breaks as postoperatively, the retina will detach with a risk of PVR formation. Sclerotomy-related breaks have been described in 3.1 % of eyes up to 10 years after the surgery and in a further 2.9 % thereafter (Al-Harthi et al. 2005).
Some surgeons advocate the use of 360¡ laser to reduce postoperative RRD (from 13 to 3 % in one study although these would appear to be high rates of postoperative RRD in routine PPV) (Koh et al. 2007). This is not routinely recommended, and it is better to identify breaks and treat these only.
Fig. 2.39 Hitting the retina with an instrument can lead to a severe localised injury to the retina as in this patient where a momentÕs inattention by the surgeon has allowed an instrument to drift posteriorly and scrape the retina. Always be aware of the position of your instruments in the vitreous cavity; if you are distracted during surgery, pull the instrumentsÕ tips anteriorly towards the sclerotomy sites
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2.13.7 Hypotony
Hypotony can occur from leaking sclerotomies. This is unusual with sutured wounds 0.3 % (Stein et al. 2009) but is more common with self-sealing or small gauge surgery. Also check any cataract extraction wounds. Postoperative hypotony can vary from mild reduction in IOP to choroidal effusions to collapse of the sclera. Mild cases can be monitored and the IOP will increase over a week or two. Severe cases, for example, with scleral infolding require closure of the leaking wound and reinßation of the eye.
2.13.8 Scleritis
Be wary of any inßammation around sclerotomy sites. Absorbable sutures can create an inßammatory reaction especially if they are protruding or on the surface of the conjunctiva. If there is a scleritis response, it is worth considering using systemic antibiotics in case there is an infection as the cause. Infectious scleritis has been described with Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (Rich et al. 2008). An occasional patient may be seen with scleromalacia; the only patients I have seen like this have been lost to follow-up and returned at 6 months with the complication. I have presumed that noncompliance with postoperative medication has caused inßammation and scleritis resulting in the scleromalacia. Surgically induced necrotising scleritis (STNS) has been described (Morley and Pavesio 2008). This is associated with systemic autoimmune disease. Indeed necrotising scleritis has been described years after surgery at the sites of surgical wounds in patients with systemic autoimmune disease. Scleritis of this sort will require systemic immunosuppressive therapy.
Scleritis can occur in relation to scleral buckles.
2.13.9 Sympathetic Uveitis
This is a rare occurrence after vitrectomy. The risk has been described as high as 1 in 500 after PPV in a surveillance survey in the UK (Kilmartin et al. 2000a, b). However, I have not seen a case in 6000 vitrectomies, and I doubt this high a prevalence. The condition is characterised by a panuveitis see Chap. 15.
Table 2.4 Potential complications from pars plana vitrectomy
Postoperative complications of vitrectomy
Anterior segment |
Cataract |
|
Glaucoma |
|
Conjunctival scarring |
|
Subconjunctival haemorrhage |
|
Scleritis |
|
Corneal endothelial loss |
|
Corneal epithelial erosion |
|
Sclerotomy leakage |
|
Sclerotomy inßammation |
|
Sclerotomy infection |
|
Uveitis |
|
Toxic anterior segment syndrome |
Posterior segment |
Endophthalmitis |
|
Choroidal haemorrhage |
|
Retinal detachment |
|
Epiretinal membrane |
|
Proliferative vitreoretinopathy |
Other |
Diplopia |
|
Surgically induced scleritis |
|
Sympathetic ophthalmitis |
|
Phthisis bulbi |
Fig. 2.40 If a patient develops hypopyon and inßammation on the Þrst day postoperatively, this may indicate toxic anterior segment syndrome as in this eye with combined PPV and Phaco. This may occur from contamination of the intraocular lens, other instruments and equipment. You may need to treat as infective with vitreous biopsy and intravitreal antibiotics, but the condition will clear in a week with topical steroids. Unfortunately, if severe, complications such as cystoid macular oedema may reduce vision
