- •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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glaucoma.13,20 Before anti-VEGF drugs were available, preoperative scatter laser with the laser indirect ophthalmoscope was recommended to avoid the inability to apply laser due to the heavy fibrinous iritis that sometimes occurs in such eyes after cataract surgery.13 Currently, an intravitreal injection of bevacizumab can be given shortly before anticipated cataract surgery and PRP laser applied shortly after surgery as an office procedure.
More recently, worry has shifted from NVI to induced DME. Suto and colleagues reported that patients with simultaneous severe NPDR or early PDR and visually significant cataracts had a statistically significant higher rate of attaining 20/40 vision and lower rate of DME progression postoperatively if the order of interventions was cataract surgery first followed by PRP 3 months postoperatively compared to the alternative order of PRP first followed by cataract surgery 1–3 months later.10 Rates of application of focal/grid laser for DME were lower in the surgery first group. Eyes in the study were mixed with regard to presence or absence of DME, and if DME was present, focal laser was used before PRP was performed in the PRP group and shortly after cataract surgery in the cataract surgery first group. Breakdown of the blood–aqueous barrier was higher in the PRP first group based on aqueous flare intensity measurement.10 As this study did not use OCT, it is possible that CSME existed simultaneously with the cataract in a significant proportion of eyes, and that the PRP exacerbated this DME more than cataract surgery did.
10.12Management of Cataract in Patients with Diabetic Retinopathy Undergoing Vitrectomy
Some patients undergoing vitrectomy surgery for various indications have concomitant cataract that
interferes with the ability to achieve the goals of the vitrectomy surgery.120,121 In such cases, possible
management options include standard phacoemulsification cataract extraction with intraocular lens implantation followed by a second vitrectomy procedure at a later time or combined operations in
which both the cataract surgery and the vitrectomy are completed with a single anesthesia. There are many variations on the theme of combined surgery. For example, the cataract extraction may be done first without insertion of the intraocular lens, followed by the vitrectomy, and lastly insertion of the implant. Alternatively, a complete cataract
procedure with implant insertion may be done first followed by the vitrectomy.39,120 One or two
surgeons may be involved, usually based on cultural differences. In the United States, retinologists rarely perform cataract surgery and sequential or two-surgeon single combined procedures are more common.120 Outside the United States, it is common for retinologists to perform cataract surgery and retina surgery, and single-surgeon combined procedures are more common. Visual acuity results depend on the underlying severity of the
retinal disease. Rates of visual acuity 20/40 have been reported from 7 to 29%.120,121 In the
era before endophotocoagulation, vitrectomy surgery for complications of PDR was associated with postoperative NVI in 20–30% of cases, and simultaneous cataract extraction (lensectomy) increased the rate two to three times compared to vitrectomy without simultaneous cataract extraction.50 Application of complete panretinal endophotocoagulation at the time of vitrectomy and use of intraocular anti-VEGF drugs as surgical adjuncts have reduced this effect of concomitant cataract extraction dramatically.122 There is evidence from one case series that in the contemporary era of vitreoretinal surgery with endophotocoagulation capability reoperation rates are decreased when the crystalline lens has been removed before or during the vitrectomy procedure. The hypothesis advanced for this result is that more complete epiretinal proliferation resection and endophotocoagulation are possible in an eye without the crystalline lens.122
10.13Influence of Vitrectomy Surgery on Cataract Formation
The traditional teaching has been that vitrectomy surgery for any indication increases the rate of development of cataract. In a recent series of cases
10 Cataract Surgery and Diabetic Retinopathy |
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undergoing vitrectomy for complications of diabetic retinopathy, 49.1% of 72 phakic eyes developed significant cataract within 6 months of vitrectomy and 23.7% of phakic eyes underwent cataract extraction with intraocular lens implantation over a mean fol- low-up of 9.6 months, which would tend to support traditional teaching.122 Hutton and colleagues analyzed a retrospective series of 289 phakic eyes that had been subjected to diabetic vitrectomy. Moderate to severe cataract developed in 37% of eyes at an average of 1.1 years after surgery.54 On the other hand, Smiddy and Feuer reported a 15% incidence of cataract extraction 2 years after diabetic vitrectomy compared to 53–66% rates for comparative cohorts of eyes undergoing vitrectomy for macular pucker and macular hole, respectively, and the
rates in diabetic eyes remained significantly lower after statistically adjusting for the effect of age.123 The issue remains controversial and unresolved.
10.14Summary Flow Chart
of Management Principles and Estimated Outcomes for Diabetic Eyes Facing Cataract Surgery
A summary of management principles and average outcomes when cataract surgery is contemplated in a patient with diabetes is illustrated in the flow charts in Figs. 10.5 and 10.6.
Fig. 10.5 Flow chart with suggested management of an eye with cataract in a patient with diabetes and less than proliferative retinopathy. Average outcomes by retinopathy classification group are indicated. Reproduced with permission from Fineman and Benson36
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Fig. 10.6 Flow chart with suggested management of an eye with cataract in a patient with diabetes and proliferative retinopathy that is active or regressed. Average outcomes by retinopathy classification group are indicated.
Reproduced with permission from Fineman and Benson36. CE ¼ cataract extraction, IOL ¼ intraocular lens, implantation, VTX ¼ vitrectomy, Intraop ¼ intraoperative.
10.15Postoperative Endophthalmitis in Patients with Diabetic Retinopathy
There is some controversy regarding whether patients with diabetes undergoing cataract surgery develop
endophthalmitis at a higher rate than nondiabetics.36,124,125 The severity of diabetic retinopathy
and diabetic macular edema are exacerbated by endophthalmitis, however, and it is generally agreed
that visual results after endophthalmitis in diabetic eyes are worse than in nondiabetic eyes.61,126 The rates
ofachieving 20/40visualacuityafterendophthalmitis are 39% and 55% for diabetic and nondiabetic eyes, respectively, and similar worse outcomes for diabetic eyes were found at every level of visual acuity.126 Diabeticeyessufferingendophthalmitishavehigherratesof culture positivity, have higher rates of growth of coagulase negative staphylococci, and respond less well to
therapy, requiring more frequent additional injections and other procedures to manage the endophthalmitis.126 There is a suggestion that visual acuity outcomes are improved in eyes of diabetics suffering endophthalmitis and having visual acuity better than light perception if vitrectomy with intravitreal antibiotic injection is used rather than a vitreous tap with antibiotic injection, a result not found in nondiabetic eyes.126 Not enough
eyeswerestudiedtoallowamoredefinitivestatementto be made. 126
10.16 Summary of Key Points
Eyes of patients with diabetes have a pre-existing tendency toward vascular endothelial hyperpermeability. The effects of normal postsurgical inflammation are therefore superimposed on a diathesis for macular edema. Moreover, eyes of patients with diabetes have higher levels of
10 Cataract Surgery and Diabetic Retinopathy |
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postsurgical inflammation even after technically perfect surgery. The net effect is a higher rate of postoperative clinical and subclinical macular edema in diabetic eyes.
It is difficult to distinguish a PCME component from a DME component of macular thickening after cataract surgery in eyes of diabetics. Disk hyperfluorescence and a petalloid pattern of fluorescein leakage are not specific for PCME.
The practical consequence of the above considerations is that all eyes of diabetic patients about to undergo cataract surgery need to have a painstaking examination of the macula both clinically and by OCT. If any macular thickening is detected, every effort should be made to eliminate it before cataract surgery. This may involve focal/grid laser and use of peribulbar and intraocular steroids or intraocular anti-VEGF drugs.
Careful examination of the macula after cataract surgery is also important, and treatment should be applied promptly for macular thickening that might have been precluded by a suboptimal view through the cataract.
Complicated cataract surgery is a particularly negative influence relative to both DME and PCME; thus, cataract surgery in patients with diabetes is best performed by surgeons with low complication rates and specifically not by beginning residents.
If cataract surgery in a patient with diabetes is complicated, the early involvement of a retina specialist is worthwhile to facilitate detection of retinopathy progression and induction or worsening of DME.
Preoperative discussions of prognosis before cataract surgery are more complex in patients with diabetic retinopathy and expectations of patients need to be appropriately modulated based on the pertinent risk factors.
Active PDR at the time of cataract surgery is particularly dangerous, as it can be associated with heavy fibrinous iritis and pupillary membrane formation after surgery. Early postoperative scatter laser should be considered in such cases when preoperative treatment is not possible, and preoperative intravitreal injection of anti-VEGF drugs is prudent.
10.17 Future Directions
Further investigations are needed to resolve several questions.
1.How often do cataract surgeons misassess the presence or absence of DME in their patients being considered for cataract surgery? Should preoperative assessment for DME by a retina specialist become a standard in patients with diabetic retinopathy?
2.What is the rate of development of DME in patients without DME who undergo cataract surgery?
3.What is the rate of development of worsened DME in patients with mild DME who undergo cataract surgery?
4.Do pharmacologic or combined pharmacologic and laser treatments reduce the rate of DME worsening in patients with refractory DME undergoing cataract surgery?
5.In patients with DME and a poor macular view, what management plan produces the best visual acuity outcomes?
6.In patients with DME associated with a taut posterior hyaloid, which management plan produces the best visual acuity outcomes?
7.Does vitrectomy surgery in a diabetic patient accelerate cataract formation as it does in a nondiabetic patient?
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