- •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
D.J. Browning
Preoperative and postoperative macular thickness in eyes of diabetics undergoing uncomplicated cataract surgery
|
Mean DR |
N |
Mean preop macular thickness – |
Mean 1–2 months postop macular |
|
Study |
severity |
(eyes) |
SD (mm) |
thickness – SD (mm) |
|
Kim77 |
1.3 |
46 |
205 |
– 39 |
274 – 91 |
Kim93 |
1.0 |
50 |
275* |
322* |
|
Escaravage70 |
1.0 |
30 |
221 |
– 50 |
260 – 68 |
Hayashi102 |
0 |
34 |
170 |
– 29** |
180 – 36 |
DR = diabetic retinopathy; Preop = preoperative; Postop = postoperative; *= the SD was not stated.**= the value was the foveal thickness rather than the central subfield mean thickness. Retinopathy severity is defined as follows: 0 = no retinopathy; 1 = mild to moderate NPRD; 2 = severe NPRD. Fractional gradings between these integer values arise from calculating the mean severity for the sample of eyes in the respective studies.
From these studies, one might hazard the following synthesis of the relationship of cataract surgery and DME. Eyes of diabetic patients have a predisposition to breakdown of the blood–retina barrier. Preand postoperative treatment with nonsteroidal antiinflammatory drops and postoperative treatment with steroid drops are rational, but unproven to reduce rates of postoperative macular edema and improve visual outcomes. Eyes with treated and resolved DME are unlikely to undergo re-exacerba- tion with uncomplicated phacoemulsification cataract extraction and posterior chamber intraocular lens implantation.58 Macular thickening arising de novo after uncomplicated cataract surgery often spontaneously resolves and therefore need not be immediately treated if minimal retinopathy is present, although treatment as PCME is rational.68 DME present at the time of contemplated cataract surgery is unlikely to spontaneously resolve, may get worse
after surgery, and therefore should be treated before the cataract surgery68,93 PCME occurs more com-
monly in eyes with more advanced degrees of retinopathy and therefore anti-inflammatory treatment approaches such as peribulbar or intravitreal triamcinolone have a rationale in such eyes, even if focal/grid laser is the foundation of treatment for DME.17
(the threshold level depends on the OCT machine, but for the Stratus OCT, this might be below a signal strength of 4). Others have advocated using OCT ratherthanclinicalcriteriaindecisions regardingperioperative management of DME.106 In the presence of cataract and diabetic retinopathy, it is the author’s opinion that OCT should be routinely obtained preoperatively to prevent the occurrence of a postoperative surprise of DME that was present but unsuspected in the preoperative state. The use of fluorescein angiography has been advocated as a way to distinguish PCME from DME.9 Because the evidence is weak that the findings of disk hyperfluorescence or petalloid macular staining discriminate PCME from DME with reproducible specificity, this recommendation seems costly and imprudent.68,70
In eyes with dense cataracts preventing a view of the fundus, a useful ancillary study is iris fluorescein angiography.107 Any presence of NVI should alert the surgeon to the certain presence of severe NPDR or PDR.107 Consideration can be given to perioperative intravitreal bevacizumab injection and prompt PRP in such a case. Absence of NVI, however, is still compatible with the presence of advanced diabetic retinopathy, and a careful fundus evaluation in the early postoperative period is necessary.
10.5The Role of Ancillary Testing in Managing Cataract Surgery in Eyes with Diabetic Retinopathy
TheclinicalassessmentofmildDMEineyeswithclear media is problematic, and retina specialists increas-
ingly rely on optical coherence tomography (OCT) to detect mild DME.104,105 In the presence of a cataract,
the clinical examination becomes even less reliable in thedetectionofmildmacularthickening,buttheOCT remains reliable until the signal strength drops
10.6Candidate Risk and Protective Factors for Diabetic Macular Edema Induction or Exacerbation Following Cataract Surgery and Suggested Management Actions
Review of retrospective series leads to a list of factors which have been associated with greater risk of macular edema induction or worsening in diabetic patients after cataract surgery. These include female
10 Cataract Surgery and Diabetic Retinopathy |
313 |
|
|
sex76 (and counterevidence59), obesity,76 control of diabetes with oral agents76 (and counterevidence59), control of diabetes with insulin,59 age 64,20 longer duration of diabetes,59 more severe retinopathy,25 poor control of diabetes,73 any macular edema before cataract surgery,20 complicated cataract surgery,72 and rapid control of poorly controlled blood glucose before surgery.78 Several factors have been cited as possibly protective against postoperative DME, including previous vitrectomy,54 posterior chamber intraocular lens implantation placement in the capsular bag rather than the sulcus,108 and previous macular photocoagulation.58,109 Prospective studies are needed to more definitively address which of these factors have the greatest predictive importance.
Based on these factors, specific suggestions for preventing DME following cataract surgery have been published. These include intensive preoperative
topical steroids or nonsteroidal anti-inflammatory drugs,24,48,80,95,110 delaying cataract surgery in
patients with diabetes until a more advanced visual handicap relative to nondiabetic patients,64,76 the opposite approach of operating on patients with diabetes and cataract earlier rather than later to capita-
lize on the evidence of lack of harm when diabetic retinopathy is absent or minimal,1,9,37,68 avoidance of
anterior chamber intraocular lenses,72 recusal of surgeons who have relatively high rates of posterior capsule rupture,72 avoidance of cataract surgery in patients with diabetic retinopathy by beginning-level residents,23 and scrupulous examination for DME in the preoperative examination and treatment with
laser photocoagulation before proceeding to surgery.58,76 These all seem to be reasonable suggestions,
subject to rigorous testing in better designed prospective studies, but the conflicting recommendations regarding when to operate cannot be wise. In the absence of a study addressing the issue, the author suggests that the threshold for cataract surgery be the same as for eyes of patients without diabetes – when the cataract is judged sufficiently advanced to interfere with the patient’s visual quality of life.
Suggestions for mitigating the possible effects of cataract surgery on retinopathy progression and DME include weekly or biweekly retinopathy checks for 3 months following cataract surgery,64 fluorescein angiography at 1, 3, and 6 months postcataract surgery in patients with diabetic retinopathy,64 aggressive laser photocoagulation for any
deterioration in retinopathy following cataract sur-
gery, and an intravitreal injection of bevacizumab at the time of cataract surgery.64,75 Some of these sug-
gested measures, such as biweekly checks and frequent fluorescein angiography, arose in a time of extracapsular and intracapsular surgeries, and seem excessive now, when phacoemulsification is the technique universally used. Modifications of these ideas may be worth considering for cases at particularly high risk rather than in routine uncomplicated cataract surgery in patients with diabetes. The widespread availability of OCT and its sensitivity for macular thickening make it the most important modality in analyzing diabetic eyes after cataract surgery.
10.7The Problem of Adherence to Preferred Practice Guidelines
In addition to the problem of accurately assessing the extent of cataract surgery induced or exacerbated DME and PCME, there is the practical problem of how frequently clinicians depart from delivering evi- dence-based care. There is consensus that cataract surgery should not be performed in patients with untreated DME if it can be avoided, because visual acuity outcomes are worse.41,73 Nevertheless, many ophthalmologists do not follow this recommendation (Fig. 10.4). McCarty et al. found that 10–16% of surveyed Australian ophthalmologists would remove the cataract of a patient with combined cataract and DME first and then address the DME.111 Indeed, it has been stated that problem of DME induced or exacerbated by cataract surgery is more accurately characterized as a problem of insufficient diagnostic accuracy by cataract surgeons in recognizing presence of DME or ignorance or disagreement with clinical practice guidelines.1,9,64
10.8Management of the Diabetic Eye Without Macular Edema About to Undergo Cataract Surgery
In contemporary ophthalmic practice, there is no agreement that any measures beyond usual perioperative cataract care should be used in eyes with diabetic retinopathy and no preoperative
314 |
D.J. Browning |
|
|
a |
b |
c |
d |
Fig. 10.4 Exemplary case demonstrating lack of awareness of guidelines regarding management of DME and cataract. A 65- year-old man with type 2 diabetes for 12 years and hypertension for 10 years saw his ophthalmologist with complaints of gradual blurring of the left eye for a year. The best corrected visual acuities were 20/30 and 20/200 of the right and left eyes, respectively. The ophthalmologist noted a cataract on the left but had a clear view of the macula and noted that diabetic macular edema was present. Left eye cataract surgery was done 2 days later without complication, but the visual acuity
was unchanged at the first postoperative examination. The fundus examination at this visit was identical to that of the preoperative examination. The patient was referred to the author to manage the diabetic retinopathy. Marked macular edema with lipid exudates and severe diabetic retinopathy were present of the left eye on clinical examination (a). Marked macular thickening was shown on OCT (b). Fluorescein angiography showed marked fluorescein leakage (c and d). The patient was treated with intravitreal triamcinolone injection and focal/grid photocoagulation
macular edema. Nevertheless, the evidence that subclinical macular thickening occurs after cataract surgery more often and more severely in such eyes than in the eyes of nondiabetics has led to studies of alternative approaches to perioperative management. Kim and colleagues have shown that a single posterior subtenon injection of triamcinolone is associated with a statistically significant decrease in OCT-measured macular thickening and best corrected visual acuity at 1 month but not 6 months.77
10.9Treatment of Diabetic Macular Edema Detected Before Cataract Surgery When the Macular View Is Clear
The most effective treatment for DME in general is focal/grid laser photocoagulation.98,112 In refractory cases, adjunctive modalities such as peribulbar triamcinolone injection, intravitreal triamcinolone injection, intravitreal injection of anti-VEGF drugs, and
10 Cataract Surgery and Diabetic Retinopathy |
315 |
|
|
sometimes vitrectomy surgery can be employed.113–115 The best order of intervention is an active area of research and remains unclear.116 Sometimes the cataract obscures the view for delivery of laser photocoagulation. In such cases, pharmacologic therapy can be used to reduce macular edema preoperatively, and prompt focal/grid laser treatment can be provided in the early postoperative period. If a taut hyaloid is present and is considered to be etiologic, a combined cataract operation with pars plana vitrectomy may be a reasonable option.
10.10Management When Cataract Sufficient to Obscure the Macular View and DME Coexist or When Refractory DME and Cataract Coexist
There is no debate regarding the management of eyes with concomitant cataract and DME when an excellent view to the macula is present. In these eyes, it should be treated and the edema should have resolved before proceeding with the cataract surgery.96 However, there are cases in which DME is present but the cataract precludes an adequate view to the macula to allow treatment of the DME or in which DME refractory to maximal focal/grid laser treatment exists. In these cases, there are several management options; the option associated with the best visual outcome is unknown. If submaximal focal/grid photocoagulation has been applied, the possible options include preoperative injection of peribulbar or intravitreal triamcinolone or bevacizumab followed by focal/grid laser photocoagulation in the early postoperative period, cataract surgery with intraoperative peribulbar or intravitreal triamcinolone injection followed by focal/grid photocoagulation in the early perioperative period, or cataract surgery without preoperative pharma-
cologic treatment with focal/grid photocoagulation.68,75,96 If maximal focal/grid laser has already
been applied and refractory DME exists, the options include serial preoperative and postoperative injections of peribulbar or intravitreal triamcinolone, serial preoperative and postoperative injections of intravitreal anti-VEGF drugs, or combined
cataract and vitrectomy surgery, the latter of which may include an array of possible steps including internal limiting membrane peeling, panretinal laser photocoagulation, and intravitreal injection with triamcinolone or anti-VEGF drugs. An example of the clinical management of refractory DME and cataract was shown in Fig. 10.2.
When DME exists and a taut posterior vitreous hyaloid is also determined to be present, consideration may be given to a combined procedure involving both phacoemulsification cataract surgery and vitrectomy with separation of the tautly adherent posterior hyaloid. The indications for this procedure are controversial even when the complicating factor of a visually significant cataract is not present. The reader is referred to Chapter 7 for perspective on this controversy. Here, we will emphasize the variables associated with combining vitrectomy and cataract surgery. Combined phacoemulsification cataract extraction and pars
plana vitrectomy is a widely practiced techni- que.117–119 All variations of the technique employ
removal of posterior hyaloid. Variations include removal of the internal limiting membrane, either aided by staining with indocyanine green or marked by triamcinolone, with or without panretinal laser treatment and with or without adjunctive intravitreal triamcinolone or anti-VEGF drugs. The disadvantages of combined surgery include increased operative time, possible need for two surgeons, and potential for increased fibrin response in the postoperative period.118 Prospective studies are needed to determine the management choices associated with the best outcomes.
10.11Patients with Simultaneous Indications for Panretinal Photocoagulation and Cataract Surgery
Traditionally, it has been taught that eyes with severe NPDR and PDR concomitant with cataract be treated with PRP first, and that cataract surgery
be deferred until angiogenically active retinopathy has been rendered quiescent.13,20 The greatest fear
in these earlier studies was NVI and neovascular
