- •Diabetic Retinopathy
- •Preface
- •Acknowledgments
- •Contents
- •Contributors
- •Pathophysiology of Diabetic Retinopathy
- •1.1 Retinal Anatomy
- •1.1.1 History
- •1.1.2 Anatomy
- •1.1.3 Microanatomy of the Retina Neurons
- •1.1.4 Intercellular Spaces
- •1.1.5 Internal Limiting Membrane
- •1.1.6 Circulation
- •1.1.7 Arteries
- •1.1.8 Veins
- •1.1.9 Capillaries
- •1.2 Hemodynamics, Macular Edema, and Starling’s Law
- •1.3 Biochemical Basis for Diabetic Retinopathy
- •1.3.1 Increased Polyol Pathway Flux
- •1.3.2 Advanced Glycation End Products (AGEs)
- •1.3.3 Activation of Protein Kinase C (PKC)
- •1.3.4 Increased Hexosamine Pathway Flux
- •1.4 Macular Edema
- •1.5 Development of Proliferative Diabetic Retinopathy
- •1.6 Summary of Key Points
- •1.7 Future Directions
- •References
- •Genetics and Diabetic Retinopathy
- •2.1 Background for Clinical Genetics
- •2.2 The Role of Polymorphisms in Genetic Studies
- •2.3 Types of Genetic Study Design
- •2.4 Studies of the Genetics of Diabetic Retinopathy
- •2.4.1 Clinical Studies
- •2.4.2 Molecular Genetic Studies
- •2.4.3 EPO Promoter
- •2.4.4 Aldose Reductase Gene
- •2.4.5 VEGF Gene
- •2.5 Genes in or Near the HLA Locus
- •2.6 Receptor for Advanced Glycation End Products (RAGE) Genes
- •2.7 Endothelial NOS2 and NOS3 Genes
- •2.9 Solute Carrier Family 2 (Facilitated Glucose Transporter), Member 1 Gene (SLC2A1)
- •2.11 Potential Value of Identifying Genetic Associations with Diabetic Retinopathy
- •2.12 Summary of Key Points
- •2.13 Future Directions
- •Glossary
- •References
- •Epidemiology of Diabetic Retinopathy
- •3.1 Introduction and Definitions
- •3.2 Epidemiology of Diabetes Mellitus
- •3.3 Factors Influencing the Prevalence of Diabetes Mellitus
- •3.4 Epidemiology of Diabetic Retinopathy
- •3.5 Diabetes and Visual Loss
- •3.6 Prevalence and Incidence of Diabetic Retinopathy
- •3.7 By Diabetes Type
- •3.8 By Insulin Use
- •3.10 By Duration of Diabetes Mellitus
- •3.11 By Ethnicity
- •3.12 Gender
- •3.13 Age at Onset of Diabetes
- •3.14 Socioeconomic Status and Educational Level
- •3.15 Family History of Diabetes
- •3.16 Changes Over Time
- •3.17 Epidemiology of Diabetic Macular Edema (DME)
- •3.18 Epidemiology of Proliferative Diabetic Retinopathy (PDR)
- •3.19 Socioeconomic Impact of Diabetes
- •3.20 Socioeconomic Impact of Diabetic Retinopathy
- •3.21 Summary of Key Points
- •3.22 Future Directions
- •References
- •Systemic and Ocular Factors Influencing Diabetic Retinopathy
- •4.1 Introduction
- •4.2 Systemic Factors
- •4.2.1 Glycemic Control
- •4.2.1.1 Type 1 Diabetes Mellitus
- •4.2.1.2 Type 2 Diabetes Mellitus
- •4.2.1.3 Rapidity of Improvement in Glycemic Control
- •4.2.2 Glycemic Variability
- •4.2.3 Insulin Use in Type 2 Diabetes
- •4.2.5 Blood Pressure
- •4.2.6 Serum Lipids
- •4.2.7 Anemia
- •4.2.8 Nephropathy
- •4.2.9 Pregnancy
- •4.2.10 Other Systemic Factors
- •4.2.11 Influence on Visual Loss
- •4.3 Effects of Systemic Drugs
- •4.3.1 Diuretics
- •4.3.3 Aldose Reductase Inhibitors
- •4.3.4 Drugs That Target Platelets
- •4.3.5 Statins
- •4.3.6 Protein Kinase C Inhibitors
- •4.3.7 Thiazolidinediones (Glitazones)
- •4.3.8 Miscellaneous Drugs
- •4.4 Ocular Factors Influencing Diabetic Retinopathy
- •4.6 Economic Consequences
- •4.7 Summary of Key Points
- •4.8 Future Directions
- •References
- •Defining Diabetic Retinopathy Severity
- •5.1 Summary of Key Points
- •5.2 Future Directions
- •5.3 Practice Exercises
- •References
- •6.1 Optical Coherence Tomography (OCT)
- •6.2 Heidelberg Retinal Tomograph (HRT)
- •6.3 Retinal Thickness Analyzer (RTA)
- •6.4 Microperimetry
- •6.5 Color Fundus Photography
- •6.6 Fluorescein Angiography
- •6.7 Ultrasonography
- •6.8 Multifocal ERG
- •6.9 Miscellaneous Modalities
- •6.10 Summary of Key Points
- •6.11 Future Directions
- •6.12 Practice Exercises
- •References
- •Diabetic Macular Edema
- •7.1 Epidemiology and Risk Factors
- •7.2 Pathophysiology and Pathoanatomy
- •7.2.1 Anatomy
- •7.3 Physiology
- •7.4 Clinical Definitions
- •7.5 Focal and Diffuse Diabetic Macular Edema
- •7.6 Subclinical Diabetic Macular Edema
- •7.7 Refractory Diabetic Macular Edema
- •7.8 Regressed Diabetic Macular Edema
- •7.9 Recurrent Diabetic Macular Edema
- •7.10 Methods of Detection of Diabetic Macular Edema
- •7.11 Case Report 1
- •7.12 Case Report 2
- •7.13 Other Ancillary Studies in Diabetic Macular Edema
- •7.14 Natural History
- •7.15 Treatments
- •7.15.1 Metabolic Control and Effects of Drugs
- •7.16 Focal/Grid Laser Photocoagulation
- •7.16.1 ETDRS Treatment of CSME
- •7.17 Evolution in Focal/Grid Laser Treatment Since the ETDRS
- •7.18 Macular Thickness Outcomes After Focal/Grid Photocoagulation
- •7.19 Resolution of Lipid Exudates After Focal/Grid Laser Photocoagulation
- •7.20 Inconsistency in Defining Refractory Diabetic Macular Edema
- •7.21 Alternative Forms of Laser Treatment for Diabetic Macular Edema
- •7.22 Peribulbar Triamcinolone Injection
- •7.23 Intravitreal Triamcinolone Injection
- •7.24 Intravitreal Dexamethasone Delivery System
- •7.27 Combined Intravitreal and Peribulbar Triamcinolone and Focal Laser Therapy
- •7.28 Vitrectomy
- •7.29 Supplemental Oxygen and Hyperbaric Oxygenation
- •7.30 Resection of Subfoveal Hard Exudates
- •7.31 Subclinical Diabetic Macular Edema
- •7.32 Cases with Simultaneous Indications for Focal and Scatter Laser Photocoagulation
- •7.34 Factors Influencing Treatment of Diabetic Macular Edema
- •7.35 Sequence of Therapy
- •7.36 Interaction of Cataract Surgery and Diabetic Macular Edema
- •7.37 Summary of Key Points
- •7.38 Future Directions
- •References
- •Diabetic Macular Ischemia
- •8.1 Introduction
- •8.2 Pathogenesis, Anatomy, and Physiology
- •8.3 Natural History
- •8.4 Clinical Evaluation
- •8.5 Clinical Significance of Diabetic Macular Ischemia
- •8.6 Controversies and Conundrums
- •8.7 Summary of Key Points
- •8.8 Future Directions
- •References
- •Treatment of Proliferative Diabetic Retinopathy
- •9.1 Introduction
- •9.2 Laser Photocoagulation
- •9.2.1 Indications
- •9.2.2 PRP Technique
- •9.2.3 Complications
- •9.2.4 Outcome
- •9.3 Intraocular Pharmacological Therapy
- •9.4 Vitreoretinal Surgery
- •9.4.1 Indications
- •9.4.2 Preoperative Management
- •9.4.3 Instrumentation
- •9.4.4 Techniques
- •9.4.5 Postoperative Management
- •9.4.6 Complications
- •9.4.7 General Outcome
- •9.5 Follow-Up Considerations in PDR
- •9.6.1 Cataract and PDR
- •9.6.2 Dense Vitreous Hemorrhage and Untreated PDR
- •9.6.3 Untreated PDR with Diabetic Macular Edema
- •9.6.4 PDR with Severe Fibrovascular Proliferation/Traction Retinal Detachment
- •9.6.5 PDR with Neovascular Glaucoma
- •9.6.6 Conditions Altering the Clinical Course of PDR
- •9.7 Summary of Key Points
- •9.8 Future Directions
- •References
- •Cataract Surgery and Diabetic Retinopathy
- •10.1 Scope of the Problem of Diabetic Retinopathy Concomitant with Surgical Cataract
- •10.2 Visual Outcomes After Cataract Surgery in Patients with Diabetic Retinopathy
- •10.3 Postoperative Course and Special Considerations After Cataract Surgery in Patients with Diabetic Retinopathy
- •10.4 The Influence of Cataract Surgery on Diabetic Retinopathy
- •10.5 The Role of Ancillary Testing in Managing Cataract Surgery in Eyes with Diabetic Retinopathy
- •10.6 Candidate Risk and Protective Factors for Diabetic Macular Edema Induction or Exacerbation Following Cataract Surgery and Suggested Management Actions
- •10.7 The Problem of Adherence to Preferred Practice Guidelines
- •10.8 Management of the Diabetic Eye Without Macular Edema About to Undergo Cataract Surgery
- •10.9 Treatment of Diabetic Macular Edema Detected Before Cataract Surgery When the Macular View Is Clear
- •10.10 Management When Cataract Sufficient to Obscure the Macular View and DME Coexist or When Refractory DME and Cataract Coexist
- •10.11 Patients with Simultaneous Indications for Panretinal Photocoagulation and Cataract Surgery
- •10.12 Management of Cataract in Patients with Diabetic Retinopathy Undergoing Vitrectomy
- •10.13 Influence of Vitrectomy Surgery on Cataract Formation
- •10.15 Postoperative Endophthalmitis in Patients with Diabetic Retinopathy
- •10.16 Summary of Key Points
- •10.17 Future Directions
- •References
- •The Relationship of Diabetic Retinopathy and Glaucoma
- •11.1 Interaction of Diabetes and Glaucoma
- •11.2 Iris and Angle Neovascularization Pathoanatomy and Pathophysiology
- •11.3 Epidemiology
- •11.4 Clinical Detection
- •11.5 Classification
- •11.6 Risk Factors for Iris Neovascularization
- •11.7 Entry Site Neovascularization After Pars Plana Vitrectomy
- •11.8 Anterior Hyaloidal Fibrovascular Proliferation
- •11.9 Treatments for Iris Neovascularization
- •11.10 Modifiers of Behavior of Iris Neovascularization
- •11.11 Management of Neovascular Glaucoma
- •11.12 Summary of Key Points
- •11.13 Future Directions
- •References
- •The Cornea in Diabetes Mellitus
- •12.1 Introduction
- •12.2 Pathophysiology
- •12.3 Anatomy and Morphological Changes
- •12.4 Clinical Manifestations
- •12.5 Ocular Surgery
- •12.6 Treatment of Corneal Disease in Diabetes Mellitus
- •12.7 Conclusion
- •12.8 Summary of Key Points
- •12.9 Future Directions
- •References
- •Optic Nerve Disease in Diabetes Mellitus
- •13.1 Relevant Normal Optic Nerve Anatomy and Physiology
- •13.2 The Effect of Diabetes on the Optic Nerve
- •13.3 Nonarteritic Anterior Ischemic Optic Neuropathy and Diabetes
- •13.4 Diabetic Papillopathy
- •13.5 Disk Edema Associated with Vitreous Traction
- •13.6 Superior Segmental Optic Hypoplasia (Topless Optic Disk Syndrome)
- •13.7 Wolfram Syndrome
- •13.8 Summary of Key Points
- •13.9 Future Directions
- •References
- •Screening for Diabetic Retinopathy
- •14.1 Introduction
- •14.2 Who Does Not Need to Be Screened
- •14.5 Screening with Dilated Ophthalmoscopy by Ophthalmic Technicians or Optometrists
- •14.6 Screening with Dilated Ophthalmoscopy by Ophthalmologists
- •14.7 Screening with Dilated Ophthalmoscopy by Retina Specialists
- •14.8 Photographic Screening
- •14.9 Nonmydriatic Photography
- •14.10 Mydriatic Photography
- •14.11 Risk Factors for Ungradable Photographs
- •14.12 Number of Photographic Fields
- •14.13 Criteria for Referral
- •14.14 Obstacles to the Use of Teleophthalmic Screening Methods
- •14.15 Combination Methods of Screening
- •14.16 Case Yield Rates
- •14.17 Compliance with Recommendation to Be Seen by an Ophthalmologist
- •14.18 Intravenous Fluorescein Angiography and Oral Fluorescein Angioscopy
- •14.19 Automated Fundus Image Interpretation
- •14.20 Subgroups Needing Enhanced Screening Efforts
- •14.21 Screening in Pregnancy
- •14.22 Economic Considerations
- •14.23 Comparisons of the Screening Methods
- •14.24 Accountability of Screening Programs
- •14.25 Summary of Key Points
- •14.26 Future Directions
- •References
- •Practical Concerns with Ethical Dimensions in the Management of Diabetic Retinopathy
- •15.1 Incorporating Ancillary Testing in the Management of Patients with Diabetic Retinopathy
- •15.2.1 Case 1
- •15.2.2 Case 2
- •15.4 Working in a Managed Care Environment (Capitation)
- •15.5 Interactions with Medical Industry
- •15.7 Comanagement of Patients
- •15.9 Summary of Key Points
- •15.10 Future Directions
- •References
- •Clinical Examples in Managing Diabetic Retinopathy
- •16.1.1 Discussion
- •16.2 Case 2: Bilateral Proliferative Diabetic Retinopathy with Acute Vitreous Hemorrhage in One Eye and a Chronic Traction Retinal Detachment in the Other Eye
- •16.2.1 Discussion
- •16.2.2 Opinion 1
- •16.2.3 Opinion 2
- •16.2.4 Opinion 3
- •16.3 Case 3: Sight Threatening Diabetic Retinopathy in a Patient with Concomitant Medical and Socioeconomic Problems
- •16.3.1 Discussion
- •16.4 Case 4: Asymptomatic Retinal Detachment Following Vitrectomy in a Patient Who Has Had Panretinal Laser Photocoagulation
- •16.4.1 Discussion
- •16.5 Case 5: Management of Progressive Vitreous Hemorrhage Following Scatter Photocoagulation for Proliferative Diabetic Retinopathy
- •16.5.1 Discussion
- •16.6.1 Discussion
- •16.7 Case 7: Proliferative Diabetic Retinopathy with Macular Traction and Ischemia
- •16.7.1 Discussion
- •16.8 Case 8: What Is Maximal Focal/Grid Laser Photocoagulation for Diabetic Macular Edema?
- •16.8.1 Definition of the Problem
- •16.8.2 Discussion
- •16.9 Case 9: What Independent Information Does Macular Perfusion Add to Patient Management in Diabetic Retinopathy?
- •16.9.1 Discussion
- •16.10 Case 10: Macular Edema Following Panretinal Photocoagulation for Proliferative Diabetic Retinopathy
- •16.10.1 Discussion
- •16.11 Case 11: Diabetic Macular Edema with a Subfoveal Scar
- •16.11.1 Discussion
- •16.12.1 Definition of the Problem
- •16.12.2 Discussion
- •16.13.1 Definition of the Problem
- •16.13.2 Discussion
- •16.14 Case 14: How Is Diabetic Macular Ischemia Related to Visual Acuity?
- •16.14.1 Definition of the Problem
- •16.14.2 Discussion
- •References
- •Subject Index
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sclerotomy. Silicone oil completely fills the eye and when it starts to back up into the infusion line, the air infusion pressure is dropped to 0 mmHg to facilitate the entry of silicone into infusion tubing. Enough silicone is allowed to enter the air infusion line to permit reflux back into the eye once the supratemporal sclerotomy is sutured and the air infusion pressure is set to 20 mmHg to normalize the intraocular pressure. When silicone ceases to move within the air infusion line, the infusion cannula is removed and immediately closed with the preplaced suture. When planning for the use of silicone oil in an eye with a silicone IOL, an effort is made to keep the posterior capsule intact to avoid contact between the two silicone products. In an aphakic eye an inferior iridectomy is necessary to prevent pupillary block glaucoma. A basal iridectomy is best performed prior to gas–fluid exchange and silicone injection. The tip of the vitrectomy probe is placed cutter-side up at the pupil. Remaining close to the posterior surface of the iris, the vitrectomy probe is gently directed toward the 6 o’clock position until it comes to rest in the ciliary sulcus. Very slight anterior movement of the instrument tip moves the iris forward and assures proper positioning. The vitrectomy cutter is activated on low suction and a basal iridectomy is created. Bleeding is a rare problem that can be managed by elevating IOP or by placing sodium hyaluronate into the anterior chamber.
Surgical management of neovascular glaucoma: The reader is referred to Chapter 11 for discussion.
Scleral buckle procedures: The reader is referred elsewhere on the techniques of scleral buckle placement.506 In the absence of persistent peripheral retinal traction or peripheral retinal break, a scleral buckle is usually not necessary in diabetic vitrectomy.402 Furthermore, the possibility of anterior segment ischemia from scleral buckling is best avoided in the diabetic eye.507
9.4.5 Postoperative Management
A number of postoperative concerns guide the care of the diabetic patient after vitrectomy surgery. Communication and coordination with the internist is important for optimal patient care.508 Topical antibiotics and steroids are commonly prescribed
to prevent infection and minimize inflammation. Pain control may not be an issue in straightforward cases with the use of smaller gauge instruments which do not require sutures or when conjunctival sutures knots are buried. Pain from corneal epithelial defects may be mild due to diabetic neuropathy. There in good evidence for the effectiveness of topical nonsteroidal anti-infammatory for controlling pain from traumatic corneal abrasions.509 Patching does not appear to be helpful for control of pain.510 The use of a therapeutic contact lens may improve comfort, but is not commonly employed.511 With extensive surgery pain control may warrant narcotic analgesics. Anterior segment inflammation is mild when surgery is limited to the vitreous and retina, but is treated aggressively with steroids and cycloplegics to control pain and prevent complications. Unexpected inflammation prompts concern of endophthalmitis and may require vitreous culture and antibiotic injection. Intraocular pressure is monitored and normalized to prevent pain and visual field loss. The posterior segment is evaluated on routine examinations to give assurance of proper healing and to identify complications. Preoperative traction retinal detachment may take months to resolve following successful surgery and may be monitored with ocular coherence tomography.512 Patient compliance is facilitated by the use of written instructions.513
Intravitreal gas: The need for postoperative positioning with intravitreal gas depends on the location of retinal breaks and may be facilitated with positioning pillows and tables. A sitting (head-up) position is needed to support the superior retina and face-down positioning is necessary to maximally support the posterior pole. Rarely, a patient may properly position the head to support the inferior
retina.438 Adhesion of the retina to the RPE occurs in 1–4 days after laser retinopexy.514–516 Feathering
of the crystalline lens may be minimized by facedown positioning to improve visualization of the retina in the postoperative course. Furthermore, an attempt is made to avoid prolonged face-up positioning as contact of gas with the crystalline lens promotes cataract formation. In a pseudophakic eye face-up positioning may cause iris capture, iridocorneal adhesion, or anterior synechiae. In an aphakic eye the anterior chamber may completely flatten.517 A Medic Alert Bracelet is worn by
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the patient who is advised to avoid nitrous oxide
and air travel until released by the retinal surgeon.518,519
If laser treatment is needed while a gas bubble is present, precautions may be required to avoid inadvertent retinal damage from the reflection of laser by the gas/fluid interface. Proposed methods of prevention include avoiding argon blue-green laser and efforts to minimize the angle of incidence of the laser beam with the gas–fluid interface.520
When using intravitreal gases, there is a potential for elevation of intraocular pressure. Topical antiglaucoma drops instilled at the conclusion of
surgery may reduce the incidence of damaging elevation of IOP.521,522 Topical and oral pressure
lowering medication may be continued during the postoperative period as needed. If unacceptable IOP elevation occurs in the presence of a complete gas fill, a par plana tap may be necessary to remove gas and normalize the IOP.
Silicone oil: Postoperative positioning is less critical with a complete silicone oil fill and there are no restrictions to air travel or anesthesia. Intravitreal silicone interferes with diagnostic ultrasonography
and axial length measurements for IOL calculations.523,524 Early postoperative anterior chamber
migration of silicone oil may be indicative of choroidal effusion or hemorrhage and is more common in the aphakic eye than in the phakic or pseudophakic eye with intact zonules. Delayed postoperative anterior migration of silicone oil may be indicative of proliferative vitreoretinopathy or closure of the inferior iridectomy.525 Apart from the occasional need for early removal of silicone oil in response to complications, silicone oil is routinely removed for optimal return of vision and to prevent complications associated with extended retention of oil. Extraction of silicone is performed at the surgeon’s discretion, usually in 3–6 months. Recurrent retinal detachment occurs in a minority of cases and
appears independent of duration of silicone oil tamponade.526,527 After removal of silicone oil, the inci-
dence of entopically detected residual droplets of silicone oil does not appear to be influenced by air infusion at the time of silicone removal.528 Removal of silicone is usually performed through a sclerotomy either actively or passively, but it may be removed through the anterior chamber combined with cataract surgery.528,529 Silicone is typically
removed as soon as the retina appears stable in order to prevent complications, but may be used
for long-term tamponade in severe cases to prevent
phthisis.120,330,530,531
9.4.6 Complications
Important complications of vitrectomy surgery include those associated with systemic disease and anesthesia. Untoward effects may be ocular or systemic in nature. The following is a review of ocular complications from the vitrectomy surgical procedure itself.
Conjunctival complications: Aside from the common findings of hemorrhage, edema, and inflammation from surgery, stitch abscess can progress to scleritis or endophthalmitis and may warrant continuing topical antibiotics until surface sutures have dissolved.532 Burying suture knots may decrease suture exposure and improve comfort. Careful conjunctival closure helps prevent recession and exposure of glaucoma setons and scleral exoplants. Subconjunctival granuloma from silicone oil is prevented by complete closure of sclerotomies.533
Corneal complications: Corneal complications of vitreoretinal surgery may interfere with postoperative healing and compromise final visual return. Corneal epithelial defects are common during and after vitrectomy surgery in diabetics. Poor adhesion of the epithelium to the basement membrane and
corneal neuropathy increases the susceptibility to damage.142,534 Risk factors include duration of
surgery and the use of an irrigating surgical contact lens.534 The need for intentional surgical debridement of the epithelium may be minimized by avoiding prolonged elevation of intraocular pressure during surgery. The tendency for delayed re-epithelialization and potential for infection complicates the postoperative recovery. The prompt identification and management of dellen formation due to elevation/edema of limbal conjunctiva may prevent serious complications.535 Treatment with lubricants improves comfort and antibiotic prophylaxis may prevent ulcerative keratitis. Particular care must be taken to preserve corneal epithelial integrity in post-LASIK eyes to prevent flap
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displacement.536 Corneal endothelial trauma may manifest with chronic long-term complications following vitrectomy. Causes of damage to the endothelium include contact with irrigating fluids, gas, silicone oil, and other vitreous substitutes and agents used for tamponade.534 Therefore, preventive efforts are aimed at preserving a barrier between the vitreous and the anterior chamber (the crystalline lens, lens implant, or lens capsule). Removal of silicone and perfluorocarbon liquids from the anterior chamber reduces the risk of corneal decompensation.534 Corneal astigmatism from sclerotomy incisions is usually transient and may be minimized by avoiding an excessively tight sclerotomy closure or with self-sealed, small-gauge incisions.537 The reader is referred to Chapter 12 for further discussion.
Scleral complications: Proper management of the sclerotomy site is important in preventing scleral complications. Postoperative wound leaks due to incomplete closure of a sclerotomy incision may be transient and inconsequential. However, complica-
tions include conjunctival bleb, choroidal effusion, and endophthalmitis.420,538,539 Infectious scleritis is
a rare, but serious complication.540 Fibroplasia at the scleral incision site may lead to fibrous ingrowth and contribute to the development of anterior hyaloidal fibrovascular proliferation.541 Unknown is the significance of wound closure, but persistent VEGF production from ischemic retina appears critical.542 Additional internal complications related to the sclerotomy include vitreous traction causing retinal tears, retinal detachment, and vitreous hemorrhage.541 With repeated vitrectomy procedures, scleral thinning at a previous sclerotomy site may necessitate the use of new sites for sclerotomy to avoid difficulty with closure. Severe scleral thinning that requires a tectonic graft is rare.543
Iritis and hyphema: Postoperative iritis is usually mild following vitreoretinal surgery. Significant pain and marked cellular and fibrin response is unusual and prompts consideration of infectious endophthalmitis. Pseudo-endophthalmitis may present when triamcinolone is used at surgery regardless of the phakic status of the eye. The triamcinolone crystals may form a pseudohypopyon, which is not usually associated with pain or significant fibrin. The chalkwhite appearance of the particles of varying size points toward the correct diagnosis.544
Intraoperative hyphema may occur especially with rubeosis and is controlled by elevating the IOP or with sodium hyaluronate.451 The preoperative discontinuation of anticoagulants may reduce the incidence of hyphema in high-risk cases. Postoperative hyphema is rare and may require testing for sickle hemoglobinopathy and requires strict attention to IOP control.545
Fibrinoid syndrome associated with postvitrectomy retinal detachment: The deposition of fibrin strands in the anterior chamber and vitreous may occur following vitrectomy for severe PDR. Fibrin strands may be seen initially on the surface of the retina and in the anterior chamber, potentially causing pupillary block glaucoma.339 A gelatinous mass forms in the vitreous cavity and subsequent contraction results in traction retinal detachment, rubeosis, and neovascular glaucoma.341 Fibrinoid syndrome causing retinal detachment is reported following
approximately 5% of diabetic vitrectomy procedures with mixed indications.341,341 Milder forms
of postoperative fibrin deposition are more common. Postoperative fibrin in the anterior chamber without retinal detachment is reported in 10–22% of combined vitrectomy–phacoemulsification–IOL (VPI).546,547 Fibrinous inflammatory reaction is a proposed cause of an increased incidence of posterior capsular fibrosis in this cohort.548 Postoperative fibrin is seen significantly more frequently after combined VPI when the indication for vitrectomy is diabetic retinopathy compared to non-diabetic VPI in some retrospective series549 and not in others.550 In these combined procedures, the method of cataract extraction appears to influence the incidence of fibrin formation. The rate is higher with extracapsular extraction (80%)551 and lower with pars plana lensectomy.552 Risk factors of fibrinoid syndrome with retinal detachment include poorly controlled type 1 diabetes; previous surgery for diabetic retinal detachment; and surgical risk factors of extensive surgery including scleral buckling, mem-
brane dissection, extensive PRP/cryopexy, and lensectomy.285,341,547 Approximately one-third of
affected eyes respond to high-dose systemic and topical steroids.341 Prompt resolution of fibrin is
reported with intracameral injection of tissue plasminogen activator (tPA).339,340,553 However, postinjec-
tion intraocular bleeding is common as in subsequent recurrence of the fibrinoid syndrome.553 Therefore,
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repeat injections of tPA may be needed.554 Prognosis
is poor in severe cases in which vitrectomy surgery has been attempted.284,285 Prevention of fibrin for-
mation with intravitreal steroids performed at the time of the initial surgery may be considered in high-risk cases.555
Iris/trabecular complications: Intraoperative iris manipulation is avoided to minimize postoperative iritis. However, inferior iridotomy is required in some cases (refer to section on silicone oil complications). Postoperative ocular hypertension may result from a number of causes including corticosteroid use, hyphema or diffuse blood, ghost cells, neovascularization, expansile gas, silicone oil, or suprachoroidal hemorrhage. In addition, pupillary block glaucoma may be precipitated by ciliary body edema/anterior choroidal effusion from laser/ inflammation from surgery.197 Treatment is directed at the underlying cause.
Rubeosis and neovascular glaucoma (NVG) portend very poor prognosis. In the ETDRS 74% of such eyes lost light perception.69 The incidence of new-onset NVG has been reported to be approximately 0.9–14% after vitrectomy/laser surgery with best results reported with the use of intraoperative
augmentation of anterior peripheral scatter laser.40,69,314,334,556 Factors that may be related to
reduced risk of NVG include retention of the crystalline lens, scatter laser photocoagulation (PRP), and postoperative retinal attachment. However, the sig-
nificance of lens removal as a risk factor appears to be decreased with the use of PRP.40,47,49,69,314,557,558
The new onset of rubeosis following vitrectomy
raises the suspicion of anterior hyaloidal fibrovascular proliferation or retinal detachment.342,559
Anterior hyaloidal fibrovascular proliferation (AHFVP): The spectrum of presentation of AHFVP includes the growth of neovascular tissue from the retina or sclerotomy sites onto the vitreous base, anterior retina, ciliary body, lens capsule, and/ or iris following vitrectomy for severe PDR.342 Patients may present with vitreous hemorrhage, rubeosis, peripheral retinal tractional detachment, and/or hypotony.342 Diagnosis may be confirmed
with high-resolution ultrasound biomicroscopy of the peripheral retina and ciliary body (Fig. 9.31).560,561
Risk factors for AHFVP appear to include male gender, type 1 diabetes, severe retinal ischemia/neovascularization, and previous vitreous surgery with
Fig. 9.31 Ultrasound biomicroscopic image of fibrovascular ingrowth. Soft tissue lesion with hyporeflective vascular core adherent to vitreous (reproduced with permission from Ophthalmology.561 Copyright # 2004 American Academy of Ophthalmology. All rights reserved)
placement of a scleral buckle.342 Inadequate PRP may allow for the postoperative progression of neovascularization, especially anteriorly in the vitreous
base. The origin of the anterior neovascularization may be the retina or the sclerotomy sites.407,562,563
Dilated external scleral vessels at the sclerotomy site suggest fibrovascular ingrowth.166,407,561 However,
fibrovascular ingrowth may be present in the absence of dilated external vessels.541 Peripheral retinal photocoagulation or cryopexy with or without treatment of sclerotomy sites may be useful with consideration of anterior dissection in very severe
cases in which fibrovascular membranes are associated with traction detachment.166,167,407 Dissec-
tion of membranes, lensectomy, retinectomy, scleral buckling, confluent laser/cryopexy, and silicone oil may be required.342 As the membranes are highly vascularized, preoperative intravitreal bevacizumab may be useful for short-term regression.240 As treatment is often difficult and unsuccessful, efforts toward prevention and early detection are important.285 In eyes at risk for AHFVP, consideration may be given to the application of extensive PRP with anterior extension to the ora serrata.
Lens complications: Cataract is a well-recognized complication of vitrectomy.564,565 However, visually significant cataracts may be less common following diabetic vitrectomy, compared with vitrectomy for macular pucker and macular hole. In eyes with clear lenses preoperatively, the 2-year
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cumulative rate of cataract extraction is 15, 53, and 66% for diabetic retinopathy, macular pucker, and macular hole, respectively.564 Many factors may play a causative role including light exposure from the operating room equipment, direct trauma from vitrectomy instruments, loss of antioxidant proper-
ties of formed vitreous, the irrigation fluid, and retinal tamponade.564–566 Efforts at prevention
include minimizing microscope light exposure and duration of surgery, avoiding direct instrument contact with the lens, and the use of supplemental 50% dextrose in the infusion fluid.459 Cataract surgery may be performed before, during, or after vitrectomy depending on the severity of the cataract and the status of the retina. If the cataract is mild, it is usually retained unless severe PDR requires extensive anterior dissection.407 Refer to Chapter 10 and the Section 9.6.1 later in this chapter for further discussion.
Endophthalmitis: The incidence of endophthalmitis following vitrectomy is low, but remains potentially devastating.544 Recent data suggest that there is no significant difference in the occur-
rence of endophthalmitis (0.03–0.23%) between 20and 25-gauge instruments.567,568 Others have
previously reported a higher incidence in smaller gauge (25 and 23 gauge) vitrectomy presumably
due to inadequate closure of self-sealed sclerotomy incisions.569,570 Aside from being a common indica-
tion for vitrectomy, poorly controlled diabetes may
be an independent risk factor for endophthalmitis and poor outcome.397,571,572 Preoperative antibiotic
prophylaxis, lid hygiene, improvement of blood glucose levels, and sterile technique are common prevention tactics.573 A high index of suspicion and low threshold to culture the intraocular fluids leads to early diagnosis and treatment with intravitreal antibiotics such as vancomycin and ceftazidime.570 Outcome is dependent on the infecting organism and early diagnosis/treatment.574
Phototoxicity: Light from the microscope or the internal light source must be kept to a minimum and directed away from the macula whenever possible. Phototoxicity appears related to light intensity and duration of exposure.575 Halothane anesthesia may offer protection against retinal phototoxicity.576 There appears to be no increased risk with multi- ple-illumination systems compared with singular endoillumination.577
Postoperative vitreous hemorrhage: Vitreous hemorrhage may be present immediately following vitrectomy surgery or may occur postoperatively. The incidence of vitreous hemorrhage following vitrectomy for proliferative diabetic retinopathy covers a wide range (12–79%), likely reflecting the varied indications for surgery.578,579 Persistent hemorrhage immediately following vitrectomy may be due to the release of blood from the peripheral vitreous skirt, especially in phakic eyes in which anterior vitrectomy is limited.579 Bleeding may also occur from vascular membranes transected at surgery, persistent vitreoretinal traction, or active neovascularization.342,579 Residual traction posteriorly has been described with vitreoschisis, whereby the
vitreous falsely appears to be separated from the retina at the time of vitrectomy surgery.471–473 If
all cortical vitreous is not removed from the retina during vitrectomy, postoperative vitreous hemorrhage may occur from tangential traction.580 Anterior hyaloidal fibrovascular proliferation is a well-recognized cause of recurrent postoperative vitreous hemorrhage and is discussed above. Allcause incidence of postoperative hemorrhage appears to be reduced by intraoperative PRP, regardless of the amount of preoperative PRP laser present.406 The use of intravitreal gas at the conclusion of vitrectomy is of undetermined value in decreasing the incidence of postoperative vitreous hemorrhage.579,581 The combined use of preoperative bevacizumab with postoperative gas tamponade may yield better results.582
Management of postoperative vitreous hemorrhage involves an initial period of observation. Echography is employed to monitor the retina for detachment. Elevation of IOP may complicate vitreous hemorrhage and may hasten intervention in medically uncontrollable cases.292,296 Gas–fluid exchange or fluid–fluid exchange with or without tissue plasminogen activator may clear the hemorrhage to restore vision and to allow for further evaluation of
the underlying cause of bleeding and for the addition of laser/cryopexy, if indicated.578,583,584 However,
repeat vitrectomy is often employed for the treatment of persistent traction or anterior hyaloidal fibrovascular proliferation.342,578,579
Retinal detachment: The incidence of retinal detachment (RD) after vitrectomy largely depends on the severity of preoperative PDR. It was
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reported in 4.3% of eyes operated primarily for
vitreous hemorrhage and 4–8% of eyes with mixed complications of PDR.291,314,334,585 The DRVS stu-
died 616 eyes and 12.3% in the early vitrectomy group developed RD compared to 18.8% in the deferral group.71 In eyes with extensive PRP, observation of asymptomatic peripheral retinal detachment may be an option.119 However, when postvitrectomy rhegmatogenous retinal detachment (RRD) requires additional surgery for repair, outcome may be poor. In a large retrospective review (n ¼ 484) of consecutive vitrectomy cases for complications of PDR, 18 eyes developed RRD and 10 (56% of the 18 eyes) progressed to NLP vision despite additional surgery.291
Gas-related complications: Intravitreal gas
increases the risk of cataract formation and elevation of IOP.295,586,587 Gas–lens contact may interfere with lens metabolism.588,589 Diabetic eyes may
be at increased risk of developing gas-related cataracts.590 Therefore, appropriate posturing may be helpful in minimizing the risk of cataract formation. Intraocular pressure (IOP) elevation may be due to
expansion of gas and/or shallowing of anterior chamber angle.295,591 Factors that promote gas
expansion include C3F8 mixtures exceeding 12–14%, SF6 mixtures exceeding 20%, postopera-
tive air travel, mountain travel, and nitrous oxide anesthesia.402,519,592–594 Elevated IOP due to
expanding gas often requires vitreous tap. Forward movement of the iris with shallowing or flattening
of the anterior chamber may be caused by intravitreal gas.590,591 It may result in pupillary capture of
an intraocular lens.595 If the vitreous cavity is less than 100% gas filled, the anterior chamber may deepen with face-down positioning alone, obviating the need for gas removal. However, reformation of the anterior chamber with gas or sodium hyaluronate may be needed if face-down positioning fails to deepen the chamber and early synechiae are suspected.595 Anterior chamber migration of gas may
result in corneal decompensation due to endothelial cell damage.590,596 This problem is most common in
an aphakic eye and may be prevented by retaining the lens, the lens implant, or the posterior capsule.
Silicone-related complications: An extensive list of complications have been reported in association with silicone oil, including cataract, glaucoma, and keratopathy.597 Cataract is common following
vitrectomy with silicone oil and was reported to occur in 64% of 265 eyes by 6 months. The incidence of cataract is expected to increase with time following surgery.440 The reader is referred to the section later in this chapter on management of cataract and PDR as well as Chapter 10.
The most common cause of corneal complications from silicone oil involves anterior chamber migration of oil, which is usually prevented by an intact lens, a posterior chamber lens implant, or inferior peripheral iridectomy. Extensive contact of silicone oil with the corneal endothelium over time results in corneal edema and band keratopathy and is best avoided by removal of silicone oil as soon as the retina is stable.598
Glaucoma may develop via open-angle or closedangle mechanisms. Intraocular pressure elevation was reported in 3% of 1196 eyes with silicone oil studied prospectively.440 The most common mechanism of glaucoma is blockage of the trabecular meshwork due to emulsification of silicone oil.599 The incidence of emulsification increases with duration of intraocular silicone oil retention.530 In addition, mechanical energy from phacoemulsification, phacofragmentation, and highspeed vitrectomy probes appears to cause emulsification.600 Prevention of glaucoma by early removal of silicone oil is ideal. Once open-angle glaucoma develops, the IOP is normalized with topical or surgical therapy and stabilization may occur with removal of intravitreal silicone oil and anterior chamber lavage to remove emulsified silicone oil droplets.
Pupillary block glaucoma from silicone oil is avoided with inferior peripheral iridotomy in the aphakic eye. However, continued postoperative patency may be problematic and require the use of steroids and Nd:YAG iridotomy.525,601 Iridotomy is usually not needed in phakic eyes or in eyes with posterior chamber lens implants, but may be performed by Nd:YAG laser postoperatively as needed for pupillary seclusion from synechiae or functional pupillary block.602
Silicone oil may interact adversely with lens implants. Adherence of silicone oil to a silicone intraocular lens may affect the visual outcome by altering the posterior refractive surface. An intact posterior capsule helps separate the two silicone products. If contact is unavoidable, the silicone
