Idiopathic Macular Hole

Prepared by the American Academy of Ophthalmology Retina Panel Retina Panel Members Emily Y. Chew, MD, Chair, Macula Society and Retina Society Representative William E. Benson, MD H. Culver Boldt, MD Tom S. Chang, MD Louis A. Lobes, Jr., MD Joan W. Miller, MD Timothy G. Murray, MD, American Society of Retina Specialists Representative Marco A. Zarbin, MD, PhD Leslie Hyman, PhD, Methodologist Preferred Practice Patterns Committee Members Joseph Caprioli, MD, Chair J. Bronwyn Bateman, MD Emily Y. Chew, MD Douglas E. Gaasterland, MD Sid Mandelbaum, MD Samuel Masket, MD Alice Y. Matoba, MD Donald S. Fong, MD, MPH Academy Staff Nancy Collins, RN, MPH Flora C. Lum, MD Mario Reynoso Medical Editor: Jeff Van Bueren Design: Socorro Soberano Reviewed by: Council Approved by: Board of Trustees September 2003 Copyright © 2003 American Academy of Ophthalmology ® All rights reserved

As a service to its members and the public, the American Academy of Ophthalmology has developed a series of guidelines called Preferred Practice Patterns™ that identify characteristics and components of quality eye care. The Preferred Practice Patterns are based on the best available scientific data as interpreted by panels of knowledgeable health professionals. In some instances, such as when results of carefully conducted clinical trials are available, the data are particularly persuasive and provide clear guidance. In other instances, the panels have to rely on their collective judgment and evaluation of available evidence. Preferred Practice Patterns provide guidance for the pattern of practice, not for the care of a particular individual. While they should generally meet the needs of most patients, they cannot possibly best meet the needs of all patients. Adherence to these Preferred Practice Patterns will not ensure a successful outcome in every situation. These practice patterns should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed at obtaining the best results. It may be necessary to approach different patients’ needs in different ways. The physician must make the ultimate judgment about the propriety of the care of a particular patient in light of all of the circumstances presented by that patient. The American Academy of Ophthalmology is available to assist members in resolving ethical dilemmas that arise in the course of ophthalmic practice. Preferred Practice Patterns are not medical standards to be adhered to in all individual situations. The Academy specifically disclaims any and all liability for injury or other damages of any kind, from negligence or otherwise, for any and all claims that may arise out of the use of any recommendations or other information contained herein. Innovation in medicine is essential to assure the future health of the American public, and the Academy encourages the development of new diagnostic and therapeutic methods that will improve eye care. It is essential to recognize that true medical excellence is achieved only when the patients’ needs are the foremost consideration. All Preferred Practice Patterns are reviewed by their parent panel annually or earlier if developments warrant and updated accordingly. To ensure that all Preferred Practice Patterns are current, each is valid for 5 years from the “approved by” date unless superseded by a revision.

Financial Disclosures: No proprietary interests were disclosed by members of the Preferred Practice Patterns Retina Panel for the past 3 years up to and including June 2003 for product, investment, or consulting services regarding the equipment, process, or products presented or competing equipment, process, or products presented.

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TABLE OF CONTENTS INTRODUCTION ...........................................................................................................2ORIENTATION..............................................................................................................3Entity .............................................................................................................................3Disease Definition..........................................................................................................3Patient Population .........................................................................................................3Activity ...........................................................................................................................3Purpose .........................................................................................................................3Goals .............................................................................................................................3BACKGROUND ............................................................................................................3Epidemiology and Risk Factors .....................................................................................3Natural History...............................................................................................................3PREVENTION AND EARLY DETECTION....................................................................4CARE PROCESS..........................................................................................................5Patient Outcome Criteria ...............................................................................................5Diagnosis.......................................................................................................................5

History ...................................................................................................................5Examination...........................................................................................................5Ancillary Tests .......................................................................................................5

Treatment ......................................................................................................................5Surgical Techniques ..............................................................................................5Indications for Surgery...........................................................................................6Outcomes of Surgery.............................................................................................6Predictors of Visual Results...................................................................................7Complications of Surgery ......................................................................................8

Follow-up.......................................................................................................................8Provider .........................................................................................................................9Counseling/Referral.......................................................................................................9APPENDIX 1. SUMMARY OF MAJOR RECOMMENDATIONS FOR CARE ...............9RELATED ACADEMY MATERIALS...........................................................................10REFERENCES ............................................................................................................11

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INTRODUCTION

The Preferred Practice Patterns (PPP) series of guidelines has been written on the basis of three principles.

Each Preferred Practice Pattern should be clinically relevant and specific enough to provide useful information to practitioners.

Each recommendation that is made should be given an explicit rating that shows its importance to the care process.

Each recommendation should also be given an explicit rating that shows the strength of evidence that supports the recommendation and reflects the best evidence available. In the process of preparing this document, a detailed literature search of articles in the English language was conducted on the subject of macular hole for the years 1968 to 2002. The results were reviewed by the Retina Panel and used to prepare the recommendations, which they rated in two ways. The panel first rated each recommendation according to its importance to the care process. This “importance to the care process” rating represents care that the panel thought would improve the quality of the patient’s care in a meaningful way. The ratings of importance are divided into three levels.

Level A, defined as most important Level B, defined as moderately important Level C, defined as relevant but not critical

The panel also rated each recommendation on the strength of evidence in the available literature to support the recommendation made. The “ratings of strength of evidence” also are divided into three levels.

Level I includes evidence obtained from at least one properly conducted, well-designed, randomized controlled trial. It could include meta-analyses of randomized controlled trials.

Level II includes evidence obtained from the following: Well-designed controlled trials without randomization Well-designed cohort or case-control analytic studies, preferably from more than one center Multiple-time series with or without the intervention

Level III includes evidence obtained from one of the following: Descriptive studies Case reports Reports of expert committees/organizations (e.g., PPP panel consensus with peer review)

The evidence cited is that which supports the value of the recommendation as something that should be performed to improve the quality of care. The panel believes that it is important to make available the strength of the evidence underlying the recommendation. In this way, readers can appreciate the degree of importance the committee attached to each recommendation and they can understand what type of evidence supports the recommendation. The ratings of importance and the ratings of strength of evidence are given in bracketed superscripts after each recommendation. For instance, “[A:II]” indicates a recommendation with high importance to clinical care [A], supported by sufficiently rigorous published evidence, though not by a randomized controlled trial [II]. The sections entitled Orientation and Background do not include recommendations; rather they are designed to educate and provide summary background information and rationale for the recommendations that are presented in the Care Process section. A summary of the major recommendations for care is included in Appendix 1.

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ORIENTATION

ENTITY Macular hole (ICD-9 #362.54).

DISEASE DEFINITION A macular hole is a full-thickness opening of the neurosensory retina involving the center of the fovea.

PATIENT POPULATION The patient population consists of individuals who present with symptoms or signs suggestive of idiopathic macular hole.

ACTIVITY Evaluation, differential diagnosis, and treatment of patients with idiopathic macular hole.

PURPOSE The purpose of evaluating, diagnosing, and managing patients with macular hole is to identify patients who might benefit from macular hole surgery, to inform these patients of the risks and benefits of such surgery, and to perform surgery and follow-up care in appropriate patients to maintain optimal central vision and vision-related quality of life.

GOALS Identify patients at risk for macular hole. Educate high-risk patients about symptoms of macular hole and about the need for periodic

follow-up. Inform patients of the risks and benefits of macular hole surgery. Treat appropriate patients who are at risk for visual loss from macular hole.

BACKGROUND

A macular hole is an anatomic opening in the retina that develops at the fovea. The patient experiences metamorphopsia and decreased visual acuity. Clinical details are available in recent review articles and editorials.1-5

EPIDEMIOLOGY AND RISK FACTORS Most investigators believe that macular holes may be caused by idiopathic vitreoretinal traction; case series have reported that trauma was responsible for a minority of cases.6, 7 In a case-control study, 72% of the idiopathic macular holes occurred in women and more than 50% of the macular holes occurred in patients 65 to 74 years old.8 Only 3% were found to occur in patients under age 55.8 The 5-year risk for developing a full-thickness macular hole (FTMH, defined as a Gass-type stage 3 or stage 4 macular hole, as defined below)9, 10 in the fellow eye of a patient with a FTMH in one eye is about 10% to 15%.11-15 If the fellow eye has a complete posterior vitreous detachment, the risk is less than 2% over 33 months of follow-up.13, 16

NATURAL HISTORY Macular hole formation typically evolves over a period of weeks to months through a series of stages first described by Gass.9, 10 Stage 1-A is characterized by loss of the foveal depression and a yellowish foveal spot approximately 100 to 200 microns in diameter. Recent evidence, using

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optical coherence tomography (OCT),17-22 the retinal thickness analyzer,23 scanning laser ophthalmoscopy,24 and observations made during vitrectomy,25, 26 demonstrates persistent vitreoretinal detachment, suggesting that anteroposterior vitreomacular traction is responsible. Initially, there is a localized shallow detachment of the perifoveal vitreous cortex with persistent adherence to the foveola. Vitreofoveolar traction may cause a split of the retina at the fovea (“pseudocyst”) that corresponds to the yellow spot.17 Approximately half of pseudocysts resolve completely.27, 28 A few evolve into a lamellar (partial-thickness) hole. Those pseudocysts that progress to a FTMH do so over a period of weeks to months, often passing through stage 1-B, which is characterized by a yellow ring 200 to 350 microns in diameter. Optical coherence tomography of stage 1-B holes demonstrates posterior extension of the pseudocyst with disruption of the outer retinal layer. The roof remains intact with persistent adherence of the posterior hyaloid to the retina.17, 18, 29 A stage 2 macular hole is defined clinically as a small retinal defect in the center of the yellow spot in a stage 1 macular hole. In a stage 2 macular hole, a small full-thickness retinal defect is present.17 Visual symptoms include metamorphopsia and decreased vision. Patients with stage 1 or stage 2 macular holes usually have visual acuity in the 20/25 to 20/80 range. About 75% of stage 2 macular holes progress to a full-thickness stage 3 or stage 4 macular hole.14, 30-33 Stage 3 holes are at least 300 to 400 microns in diameter. The posterior hyaloid is completely separated over the macula but is attached to the optic disc and more peripherally.17 An operculum or a flap on the posterior hyaloid over the hole may or may not be apparent clinically but usually can be seen on OCT. Stage 3 and stage 4 macular holes usually have a cuff of subretinal fluid, intraretinal edema, cysts, and in the base of the hole, they often have drusenlike deposits that probably represent macrophages at the level of the retinal pigment epithelium and that indicate the chronicity of the condition. In long-standing stage 3 holes, a rim of retinal pigment epithelium hyperplasia or depigmentation is often present at the junction between edematous or detached retina and normal-appearing, attached retina.34 Epiretinal membranes, which are uncommon in stage 1 and stage 2 holes, may be present. They are even more frequent in stage 4 holes.35 Patients with stage 3 or stage 4 macular holes usually have visual acuity in the 20/100 to 20/400 range.15, 34 A stage 3 macular hole becomes a stage 4 hole when a complete posterior vitreous detachment with a Weiss ring develops.10, 29 Stage 4 holes are usually slightly larger than stage 2 holes and often approximately 500 microns in diameter. The prognosis of untreated full-thickness macular holes is poor. Only approximately 5% will have 20/50 visual acuity or better, 55% to 58% will have 20/100 or better, and approximately 40% will have 20/200 or worse.12, 15, 34, 36, 37 In about 3% to 9% of cases, a stage 3 or stage 4 macular hole closes spontaneously.14, 15, 38, 39 If the hole does close, the visual acuity can recover dramatically. The vast majority of patients with untreated macular holes ultimately retain vision in the 20/100 to 20/400 range, with no further loss of central or peripheral vision.

PREVENTION AND EARLY DETECTION

There are no useful preventive measures known at this time. Early detection may be important for the fellow eye of affected individuals, who should be educated to assess their central vision for the early changes of metamorphopsia and mild visual decrease because the prognosis is better with surgical repair at an earlier stage, with a smaller hole, and with better preoperative vision. The use of eye protection to prevent potential trauma to the fellow eye of a patient with unilateral involvement should also be recommended.

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CARE PROCESS

PATIENT OUTCOME CRITERIA Patient outcome criteria include the following:

Prevention of visual loss and functional impairment Improvement of visual function Maintenance of quality of life

DIAGNOSIS The initial evaluation of a patient with symptoms and signs suggestive of macular hole includes all features of the comprehensive adult medical eye evaluation, with particular attention to those aspects relevant to macular hole.40 Conditions often mistaken for the various stages of macular hole include cystoid macular edema, central serous retinopathy, a subfoveolar druse, lamellar macular hole, and epiretinal membrane with pseudohole.5, 41, 42

History In general, a thorough history includes the following items, although the exact composition varies with the patient's particular problems and needs.

Duration of symptoms[A:III]

Ocular history: glaucoma or other prior eye diseases, injuries, surgery, or other treatments[A:III] Medications that may be related to macular cysts[A:III]

Examination Slit-lamp biomicroscopy of the macula and the vitreoretinal interface[A:III]

Ancillary Tests In most cases the diagnosis is made by clinical evaluation. Optical coherence tomography provides information on the anatomy of the macular hole and may aid in the diagnosis and staging.19, 43

TREATMENT Kelly and Wendel introduced the use of vitrectomy techniques to seal macular holes in 1991.44, 45 Subsequent studies have verified the benefit of surgery in appropriately selected patients.4 The surgical objective is to relieve anteroposterior or tangential vitreomacular traction and to induce glial tissue to bridge and close the hole.46, 47 Management includes informing patients with macular holes of the natural history of the condition, the risk of developing a macular hole in the fellow unaffected eye, the alternatives to surgery, the predictors of good surgical outcome, the associated adverse effects of macular hole surgery, and the benefits of such surgery.

Surgical Techniques Surgery may be performed using a variety of anesthesia techniques that include general anesthesia and local (regional) anesthesia (e.g., retrobulbar, peribulbar, periocular, sub-Tenon’s injection, and topical). Sedation may be used with local anesthesia to minimize pain, anxiety, and discomfort. The planned mode of anesthesia should be discussed with the patient so that the patient will know what to expect in terms of pain, comfort, consciousness level, and complications.[A:III] The particular strategy employed for anesthesia and sedation is generally based on the patient’s medical condition and the preferences of the surgeon and patient. Anesthesia techniques with retrobulbar or peribulbar needle injection may be associated with complications such as strabismus, globe perforation, retrobulbar hemorrhage, and macular infarction that are not seen with topical, blunt cannula, and other non-needle injection techniques.

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The surgeon should inform the patient of the relative risks, benefits, and alternatives to surgery, and in particular of the need for use of expansile intraocular gas or special patient positioning.[A:III] Patients with glaucoma should be informed of the possibility of a perioperative increase in intraocular pressure.[A:III] Nitrous oxide should not be used near the end of the procedure if general anesthesia is used. The diffusion of nitrous oxide into the vitreous causes an early decrease in the size of the intraocular gas bubble and, consequently, insufficient retinal tamponade. It is preferable that if general anesthesia is used, nitrous oxide should be avoided or else turned off before the last hour of the operation. The surgeon has the responsibility for formulating a postoperative care plan and should inform the patient of these arrangements.48 [A:III] Peeling of the internal limiting membrane (ILM) during surgery has been advocated because the ILM may act as a scaffold for cellular proliferation that can cause persistent vitreomacular traction, failure of the original surgery, or late reopening of initially successfully closed holes.49 Closure rates between 88% and 100% and median postoperative visual acuity as good as 20/40 have been reported with ILM peeling.50-56 However, there are no randomized controlled studies to prove the benefit of ILM peeling and there are many reports of similar results without peeling; current evidence is inconclusive. In a retrospective comparative study, there was no statistical difference in successful hole closure or postoperative visual improvement between patients who underwent preretinal/ILM peeling and those who did not.57 Some surgeons recommend visualizing the ILM with indocyanine green (ICG) dye staining to aid peeling.58, 59 There have been reports of damage to the retinal pigment epithelium with the use of ICG dye.59-63 The current evidence is inconclusive to recommend for or against the use of ICG during surgery. At this time, there is no convincing evidence that any intraoperative adjuvant improves the outcomes of vitrectomy surgery. Adjuvants studied include transforming growth factor-β2,64-66 serum,67-71 an absorbable partially cross-linked gelatin (collagen) plug,72 thrombin-activated fibrinogen,52 plasmin,73, 74 thrombin, 52, 75and a plasma-thrombin mixture. 76 Retinal tamponade is created at the end of macular hole surgery using different methods. Two early studies found better results by creating retinal tamponade with C3F8 gas than with SF6 gas.77, 78 A later study found no difference in results.79 Others have reported closure rates as high as 100% with air tamponade alone after ILM peeling.50, 53 Silicone oil has been recommended for patients who cannot be positioned or who need to travel in airplanes soon after surgery.80, 81 In one study, 86% of 40 holes were closed with this approach80 but these investigators have recently concluded that the anatomic and visual results are better with gas tamponade.82 A drawback of using silicone oil is that the patient must undergo a second operation to remove the oil. Further study is needed to determine whether maintaining a facedown position for some time after vitrectomy improves results. Some series have reported similar closure rates with no83, 84 or 1-day positioning.85, 86 There is no strong evidence for the effect on outcome of the choice of gas tamponade or duration of facedown positioning.

Indications for Surgery Surgery may be considered for patients with stage 3 and stage 4 holes.39 [A:I] The evidence for the benefits of surgery for stage 2 holes is inconclusive but surgery is generally considered in these cases to prevent progression to later stages of disease.33 [A:III] A patient with a history of a macular hole for 3 or more years may have less success with surgery and may not be a good candidate for macular hole surgery. Visual improvement in a patient with a history of a macular hole for longer than 1 year is generally modest. If the hole is larger than 400 microns in diameter, the closure rate is reduced; even if the hole can be closed, the final visual acuity is often not good. These factors should be assessed before surgery for a macular hole is recommended.[A:III]

Outcomes of Surgery It is difficult to evaluate the literature on macular hole surgery because definitions of surgical success vary; some studies considered flattening of the edges of the hole to be a surgical success while others required closure of the edges of the hole. Since reports have different lengths of follow-up, it is difficult to compare anatomic success and visual results because of cataract development and progression. Series in which most of the patients are pseudophakic may report

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better results than those in which the patients still have cataract.87 Finally, the chances of reopening of the hole increase with duration of follow-up. There are three multicenter, randomized controlled trials that provide evidence concerning the efficacy of surgery versus observation for different stages of macular hole.27, 33, 39 These small studies do not provide conclusive evidence for recommending surgery for stage 1 or stage 2 macular holes. However, the general consensus of the experts is that surgery should be considered to prevent stage 2 macular holes from progressing to stage 3 and stage 4.[A:III] De Bustros and colleagues studied patients with stage 1 macular holes. All had a FTMH in their fellow eye.27 In the observation group, 14 of 35 eyes (40%) progressed to FTMH, while in the group randomized to vitrectomy, 10 of 27 eyes (37%) progressed (P=0.81). Postoperatively, 33% of the surgery group had a visual acuity of 20/80 or worse compared with 20% of the observation group. The small number of participants limited the power of the study to detecting only large treatment effects (30%). Therefore, there is no good evidence to support surgery for stage 1 macular hole. Kim and colleagues studied patients with stage 2 macular hole.33 In the observation group, 15 of 21 eyes (71%) progressed to FTMH. Their mean Early Treatment Diabetic Retinopathy Study (ETDRS) visual acuity was 20/69 at baseline and 20/80 at 12 months. In the surgery group, 3 of 15 eyes (20%) (P=0.006) progressed to FTMH. Their mean ETDRS visual acuity was 20/60 at baseline and 20/62 at 12 months. There was no statistically significant difference in the final visual acuity (P=0.17) between the two groups. However, using the Bailey-Lovie word-reading test, the surgery group had a visual acuity of 20/78 compared with 20/135 in the observation group (P=0.006). The study results were mixed about the benefit of surgery for stage 2 macular holes. Freeman and colleagues studied patients with stage 3 and stage 4 macular holes.39 In the surgery group, 36 holes in the 52 eyes (69%) closed, as compared with 2 of 56 eyes (4%) in the observation group (P<0.001). The surgically treated eyes had statistically significantly better visual acuity at 6 months, as reflected by ETDRS chart visual acuity (20/115 vs. 20/166, P<0.004) and the Bailey-Lovie word-reading test (20/155 vs. 20/166, P<0.01). This study indicates a benefit in closure rate and final visual acuity, although the duration of follow-up was short. There were also imbalances in the mean duration of hole formation before entry into the study: 18.8 months in the surgery group and 28.6 months in the observation group. Despite these caveats, the results of this study and other case series provide evidence supporting surgery for stage 3 or stage 4 macular holes. The current anatomic success rate of vitreous surgery for idiopathic macular holes as reported in nonrandomized studies is approximately 80% to 100%.50, 53, 55, 58, 88-93 The likelihood of recovering visual acuity of 20/40 or better ranges from approximately 25% to 40%.56, 91, 94 Measures of patient satisfaction after surgery conform to the visual and anatomic results.91, 94, 95 If the initial surgery fails, 80% to 100% of holes can be closed with good visual results with additional surgery.96-99

Predictors of Visual Results Many authors have reported better closure rates and better final visual acuities if the duration of symptoms is less than 6 months.45, 50, 100-102 A macular hole that has been present longer than 2 or 3 years can be closed, but the success rate is lower (62.7%) than it is for one of shorter duration and the patient is unlikely to derive as much visual benefit from surgery.100, 103 Some studies have found that if a macular hole is larger than 300 to 400 microns in diameter, the closure rate is reduced, and even if the hole can be closed, the final visual acuity is often not good.53, 90, 104-106 Patients who have had two failed surgeries for a macular hole generally derive little or no visual benefit even if a third surgery closes the hole. However, in a series of 16 patients, if one of the previous surgeries was at least temporarily successful, the mean visual acuity improved from 20/80 to 20/40 (P=0.003).107 Less evidence exists to predict visual results for traumatic macular hole. In one series of 18 patients, 8 had spontaneous closure between 1 week and 4 months after trauma.108 Based on this

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study, observation can be considered for traumatic macular hole. When surgery is undertaken, the anatomic success rate is between 76% and 100%. The visual results vary depending on the underlying cause and duration of the macular hole, but the majority of patients have a final visual acuity of 20/50 or better.7, 109-111

Complications of Surgery The 3-year incidence of significant cataract after surgery is more than 75%.87, 112-114 Because of this high incidence, some surgeons have advocated combining macular hole surgery with phacoemulsification and placement of an intraocular lens.83, 115, 116 Such a procedure not only eliminates the need for two operations; it may also allow a more complete gas fill.83, 115 The potential complications of combining cataract surgery with vitrectomy include hypotony, intraocular lens iris capture, and increased risk of macular edema in selected patients. Corneal abnormalities may develop after the prolonged time in the operating room that may be needed to complete the surgical procedure. Up to 10% of successfully closed macular holes later reopen84, 117-121 and a 4% reopening rate after cataract surgery has been reported.116 Intraoperative retinal tears, most common inferiorly, have been reported in 3% to 17% of macular hole operations.50, 88, 119, 122-124 Postoperative retinal detachment has been reported in up to 14% of cases, but most series report an incidence of 1% to 5%.50, 52, 57, 83, 88, 112, 119, 120, 122 The detachment is typically located inferiorly and caused by small flap tears at the posterior vitreous base. Fortunately, most detachments can be repaired without reopening of the hole.124 Up to 20% of patients note temporal visual field loss after macular hole surgery,125-129 which may be caused by dehydration or by mechanical injury to the retina from air streaming from the infusion cannula toward the retina during the air–fluid exchange.130 Visual field loss potentially can be reduced by secure closure of the sclerotomies to minimize air flow through the sclerotomies during the air–fluid exchange, by leaving a large puddle of fluid posteriorly until the final aspiration,131 by humidifying the air,132 or by using a low air pressure during air–fluid exchange.133, 134 Endophthalmitis has been reported after macular hole surgery but is rare.119, 120 Patients who have retinal tamponade achieved by an expanding gas bubble will have limited options for air travel immediately following macular hole surgery when a large gas bubble (75%) is still present. Ascending to altitudes over 3000 to 4000 feet for prolonged periods may cause visual deterioration.

FOLLOW-UP The patient should be examined postoperatively within 1 or 2 days and again approximately 1 to 2 weeks after surgery.[A:III] The frequency and timing of subsequent postoperative visits varies, depending on the outcome of surgery and the patient’s symptoms. Components of the follow-up examination should include the following:

Interval history, including new symptoms[A:III]

Measurement of intraocular pressure[A:III] Slit-lamp biomicroscopy of the macula[A:III]

Patients who do not have surgery should be examined at the intervals recommended in the Comprehensive Adult Medical Eye Evaluation PPP.40 [A:III] They should be advised to contact the ophthalmologist promptly if they develop new symptoms of visual loss.[A:III] For patients with stage 1 holes, follow-up may be conducted more frequently to observe the natural course of these eyes and possibly offer timely surgery if the condition progresses to stage 2. Patients who have had a macular hole in one eye should be informed that they have a 10% to 15% chance over a period of 5 years of macular hole formation in the fellow eye if no posterior vitreous detachment is present and a 2% chance if posterior vitreous detachment is present.11-15 [A:III]

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PROVIDER Diagnosis and management of macular hole requires special expertise and skills and specialized equipment to detect alterations in the retina and the medical education and training necessary to select, perform, and monitor the appropriate treatment regimen. Consultation with or referral to an ophthalmologist who has expertise or experience in managing this condition may be desirable. The performance of certain diagnostic procedures may be delegated to appropriately trained and supervised personnel. However, the interpretation of results and the medical and surgical management of macular hole require the medical training, clinical judgment, and experience of an ophthalmologist.

COUNSELING/REFERRAL Patients should be informed to notify their ophthalmologist promptly if they have symptoms such as an increase in floaters, a loss of visual field, or a decrease in visual acuity.135-137 [A:II] Patients should be informed that air travel, high altitudes, or general anesthesia with nitrous oxide should be avoided until the gas tamponade is nearly completely gone.[A:III] Patients with functionally limiting postoperative visual impairment should be referred for vision rehabilitation and social services.138 [A:III]

APPENDIX 1. SUMMARY OF MAJOR RECOMMENDATIONS FOR CARE DIAGNOSIS

The initial evaluation of a patient with symptoms and signs suggestive of macular hole includes all features of the comprehensive adult medical eye evaluation, with particular attention to those aspects relevant to macular hole.

History In general, a thorough history includes the following items, although the exact composition varies with the patient's particular problems and needs.

Duration of symptoms[A:III]

Ocular history: glaucoma or other prior eye diseases, injuries, surgery, or other treatments[A:III] Medications that may be related to macular cysts[A:III]

Examination Slip-lamp biomicroscopy of the macula and the vitreoretinal interface[A:III]

TREATMENT Surgery may be considered for patients with stage 3 and stage 4 holes.[A:I] The evidence for the benefits of surgery for stage 2 holes is inconclusive but surgery is generally considered in these cases to prevent progression to later stages of disease.[A:III] The surgeon should inform the patient of the relative risks, benefits, and alternatives to surgery, and in particular of the need for use of expansile intraocular gas or special patient positioning.[A:III] The surgeon has the responsibility for formulating a postoperative care plan and should inform the patient of these arrangements.[A:III]

FOLLOW-UP The patient should be examined postoperatively within 1 or 2 days and again approximately 1 to 2 weeks after surgery.[A:III] The frequency and timing of subsequent postoperative visits varies, depending on the outcome of surgery and the symptoms the patient has. Components of the follow-up examination should include the following:

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Interval history, including new symptoms[A:III]

Measurement of intraocular pressure[A:III] Slit-lamp biomicroscopy of the macula[A:III]

Patients who do not have surgery should be examined at the intervals recommended in the Comprehensive Adult Medical Eye Evaluation PPP.[A:III] They should be advised to contact the ophthalmologist promptly if they develop new symptoms of visual loss.[A:III] For patients with stage 1 holes, follow-up may be conducted more frequently to observe the natural course of these eyes and possibly offer timely surgery if the condition progresses to stage 2. Patients who have had a macular hole in one eye should be informed that they have a 10% to 15% chance over a period of 5 years of macular hole formation in the fellow eye if no posterior vitreous detachment is present and a 2% chance if posterior vitreous detachment is present.[A:III]

PROVIDER Consultation with or referral to an ophthalmologist who has expertise or experience in managing this condition may be desirable.

COUNSELING/REFERRAL Patients should be informed to notify their ophthalmologist promptly if they have symptoms such as an increase in floaters, a loss of visual field, or a decrease in visual acuity.[A:II] Patients should be informed that air travel, high altitudes, or general anesthesia with nitrous oxide should be avoided until the gas tamponade is nearly completely gone.[A:III] Patients with glaucoma should be informed of the possibility of a perioperative increase in intraocular pressure.[A:III] Patients with functionally limiting postoperative visual impairment should be referred for vision rehabilitation and social services.[A:III]

RELATED ACADEMY MATERIALS

Basic and Clinical Science Course Retina and Vitreous (Section 12, 2003-2004). Complementary Therapy Assessments Surgical Management of Macular Holes (2001). Eye Fact Sheets Macular Hole (2002). Focal Points Evaluation and Management of Macular Hole (2003). LEO Clinical Topic Update Online Retina and Vitreous (2000). http://www.aao.org/education LEO Clinical Update Course CD-ROM Retina (2003). Ophthalmic Technology Assessments Surgical Management of Macular Holes (2001).

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REFERENCES

1. Colucciello MM. Focal Point: Macular Hole. In. San Francisco: American Academy of Ophthalmology, 2003.

2. Kuhn F. Point: to peel or not to peel, that is the question. Ophthalmology 2002;109:9-11.

3. Hassan TS, Williams GA. Counterpoint: to peel or not to peel: is that the question? Ophthalmology 2002;109:11-2.

4. Benson WE, Cruickshanks KC, Fong DS, et al. Surgical management of macular holes: a report by the American Academy of Ophthalmology. Ophthalmology 2001;108:1328-35.

5. Ho AC, Guyer DR, Fine SL. Macular hole. Surv Ophthalmol 1998;42:393-416.

6. Aaberg TM, Blair CJ, Gass JD. Macular holes. Am J Ophthalmol 1970;69:555-62.

7. Kuhn F, Morris R, Mester V, Witherspoon CD. Internal limiting membrane removal for traumatic macular holes. Ophthalmic Surg Lasers 2001;32:308-15.

8. Risk factors for idiopathic macular holes. The Eye Disease Case-Control Study Group. Am J Ophthalmol 1994;118:754-61.

9. Gass JD. Idiopathic senile macular hole. Its early stages and pathogenesis. Arch Ophthalmol 1988;106:629-39.

10. Gass JD. Reappraisal of biomicroscopic classification of stages of development of a macular hole. Am J Ophthalmol 1995;119:752-9.

11. Ezra E, Wells JA, Gray RH, et al. Incidence of idiopathic full-thickness macular holes in fellow eyes. A 5-year prospective natural history study. Ophthalmology 1998;105:353-9.

12. Lewis ML, Cohen SM, Smiddy WE, Gass JD. Bilaterality of idiopathic macular holes. Graefes Arch Clin Exp Ophthalmol 1996;234:241-5.

13. Fisher YL, Slakter JS, Yannuzzi LA, Guyer DR. A prospective natural history study and kinetic ultrasound evaluation of idiopathic macular holes. Ophthalmology 1994;101:5-11.

14. Guyer DR, de Bustros S, Diener-West M, Fine SL. Observations on patients with idiopathic macular holes and cysts. Arch Ophthalmol 1992;110:1264-8.

15. Chew EY, Sperduto RD, Hiller R, et al. Clinical course of macular holes: the Eye Disease Case-Control Study. Arch Ophthalmol 1999;117:242-6.

16. Akiba J, Quiroz MA, Trempe CL. Role of posterior vitreous detachment in idiopathic macular holes. Ophthalmology 1990;97:1610-3.

17. Gaudric A, Haouchine B, Massin P, et al. Macular hole formation: new data provided by optical coherence tomography. Arch Ophthalmol 1999;117:744-51.

18. Haouchine B, Massin P, Gaudric A. Foveal pseudocyst as the first step in macular hole formation: a prospective study by optical coherence tomography. Ophthalmology 2001;108:15-22.

19. Hee MR, Puliafito CA, Wong C, et al. Optical coherence tomography of macular holes. Ophthalmology 1995;102:748-56.

20. Ansari H, Rodriguez-Coleman H, Langton K, Chang S. Spontaneous resolution of bilateral stage 1 macular holes documented by optical coherence tomography. Am J Ophthalmol 2002;134:447-9.

21. Stalmans P, Spileers W, Dralands L. The use of optical coherence tomography in macular diseases. Bull Soc Belge Ophtalmol 1999;272:15-30.

11

=

22. Spaide RF, Wong D, Fisher Y, Goldbaum M. Correlation of vitreous attachment and foveal deformation in early macular hole states. Am J Ophthalmol 2002;133:226-9.

23. Folk JC, Boldt HC, Keenum DG. Foveal cysts: a premacular hole condition associated with vitreous traction. Arch Ophthalmol 1998;116:1177-83.

24. Kishi S, Kamei Y, Shimizu K. Tractional elevation of Henle's fiber layer in idiopathic macular holes. Am J Ophthalmol 1995;120:486-96.

25. Kishi S, Hagimura N, Shimizu K. The role of the premacular liquefied pocket and premacular vitreous cortex in idiopathic macular hole development. Am J Ophthalmol 1996;122:622-8.

26. Johnson MW, Van Newkirk MR, Meyer KA. Perifoveal vitreous detachment is the primary pathogenic event in idiopathic macular hole formation. Arch Ophthalmol 2001;119:215-22.

27. de Bustros S. Vitrectomy for prevention of macular holes. Results of a randomized multicenter clinical trial. Vitrectomy for Prevention of Macular Hole Study Group. Ophthalmology 1994;101:1055-9; discussion 60.

28. Johnson RN, Gass JD. Idiopathic macular holes. Observations, stages of formation, and implications for surgical intervention. Ophthalmology 1988;95:917-24.

29. Azzolini C, Patelli F, Brancato R. Correlation between optical coherence tomography data and biomicroscopic interpretation of idiopathic macular hole. Am J Ophthalmol 2001;132:348-55.

30. Hikichi T, Yoshida A, Akiba J, et al. Prognosis of stage 2 macular holes. Am J Ophthalmol 1995;119:571-5.

31. Hikichi T, Yoshida A, Akiba J, Trempe CL. Natural outcomes of stage 1, 2, 3, and 4 idiopathic macular holes. Br J Ophthalmol 1995;79:517-20.

32. Kim JW, Freeman WR, el-Haig W, et al. Baseline characteristics, natural history, and risk factors to progression in eyes with stage 2 macular holes. Results from a prospective randomized clinical trial. Vitrectomy for Macular Hole Study Group. Ophthalmology 1995;102:1818-29.

33. Kim JW, Freeman WR, Azen SP, et al. Prospective randomized trial of vitrectomy or observation for stage 2 macular holes. Vitrectomy for Macular Hole Study Group. Am J Ophthalmol 1996;121:605-14.

34. Casuso LA, Scott IU, Flynn HW, Jr., et al. Long-term follow-up of unoperated macular holes. Ophthalmology 2001;108:1150-5.

35. Blain P, Paques M, Massin P, et al. Epiretinal membranes surrounding idiopathic macular holes. Retina 1998;18:316-21.

36. Hikichi T, Trempe CL. Risk of decreased visual acuity in full-thickness idiopathic macular holes. Am J Ophthalmol 1993;116:708-12.

37. Morgan CM, Schatz H. Idiopathic macular holes. Am J Ophthalmol 1985;99:437-44.

38. Hikichi T, Akiba J, Trempe CL. Effect of the vitreous on the prognosis of full-thickness idiopathic macular hole. Am J Ophthalmol 1993;116:273-8.

39. Freeman WR, Azen SP, Kim JW, et al. Vitrectomy for the treatment of full-thickness stage 3 or 4 macular holes. Results of a multicentered randomized clinical trial. The Vitrectomy for Treatment of Macular Hole Study Group. Arch Ophthalmol 1997;115:11-21.

40. American Academy of Ophthalmology. Comprehensive Adult Medical Eye Evaluation, Preferred Practice Pattern. San Francisco: American Academy of Ophthalmology, 2000.

41. Gass JD, Joondeph BC. Observations concerning patients with suspected impending macular holes. Am J Ophthalmol 1990;109:638-46.

42. Smiddy WE, Gass JD. Masquerades of macular holes. Ophthalmic Surg 1995;26:16-24.

12

=

43. Puliafito CA, Hee MR, Lin CP, et al. Imaging of macular diseases with optical coherence tomography. Ophthalmology 1995;102:217-29.

44. Kelly NE, Wendel RT. Vitreous surgery for idiopathic macular holes. Results of a pilot study. Arch Ophthalmol 1991;109:654-9.

45. Wendel RT, Patel AC, Kelly NE, et al. Vitreous surgery for macular holes. Ophthalmology 1993;100:1671-6.

46. Rosa RH, Jr., Glaser BM, de la Cruz Z, Green WR. Clinicopathologic correlation of an untreated macular hole and a macular hole treated by vitrectomy, transforming growth factor-beta 2, and gas tamponade. Am J Ophthalmol 1996;122:853-63.

47. Madreperla SA, Geiger GL, Funata M, et al. Clinicopathologic correlation of a macular hole treated by cortical vitreous peeling and gas tamponade. Ophthalmology 1994;101:682-6.

48. American Academy of Ophthalmology. Policy Statement: An Ophthalmologist's Duties Concerning Postoperative Care. San Francisco: American Academy of Ophthalmology, 1998.

49. Eckardt C, Eckardt U, Groos S, et al. Removal of the internal limiting membrane in macular holes. Clinical and morphological findings. Ophthalmologe 1997;94:545-51.

50. Park DW, Sipperley JO, Sneed SR, et al. Macular hole surgery with internal-limiting membrane peeling and intravitreous air. Ophthalmology 1999;106:1392-7; discussion 7-8.

51. Lewis JM, Park I, Ohji M, et al. Diamond-dusted silicone cannula for epiretinal membrane separation during vitreous surgery. Am J Ophthalmol 1997;124:552-4.

52. Olsen TW, Sternberg P, Jr., Capone A, Jr., et al. Macular hole surgery using thrombin-activated fibrinogen and selective removal of the internal limiting membrane. Retina 1998;18:322-9.

53. Brooks HL, Jr. Macular hole surgery with and without internal limiting membrane peeling. Ophthalmology 2000;107:1939-48; discussion 48-9.

54. Haritoglou C, Gass CA, Schaumberger M, et al. Macular changes after peeling of the internal limiting membrane in macular hole surgery. Am J Ophthalmol 2001;132:363-8.

55. Mester V, Kuhn F. Internal limiting membrane removal in the management of full-thickness macular holes. Am J Ophthalmol 2000;129:769-77.

56. Smiddy WE, Feuer W, Cordahi G. Internal limiting membrane peeling in macular hole surgery. Ophthalmology 2001;108:1471-8.

57. Margherio RR, Margherio AR, Williams GA, et al. Effect of perifoveal tissue dissection in the management of acute idiopathic full-thickness macular holes. Arch Ophthalmol 2000;118:495-8.

58. Da Mata AP, Burk SE, Riemann CD, et al. Indocyanine green-assisted peeling of the retinal internal limiting membrane during vitrectomy surgery for macular hole repair. Ophthalmology 2001;108:1187-92.

59. Kwok AK, Li WW, Pang CP, et al. Indocyanine green staining and removal of internal limiting membrane in macular hole surgery: histology and outcome. Am J Ophthalmol 2001;132:178-83.

60. Haritoglou C, Gandorfer A, Gass CA, et al. Indocyanine green-assisted peeling of the internal limiting membrane in macular hole surgery affects visual outcome: a clinicopathologic correlation. Am J Ophthalmol 2002;134:836-41.

61. Engelbrecht NE, Freeman J, Sternberg P, Jr., et al. Retinal pigment epithelial changes after macular hole surgery with indocyanine green-assisted internal limiting membrane peeling. Am J Ophthalmol 2002;133:89-94.

62. Gandorfer A, Haritoglou C, Gass CA, et al. Indocyanine green-assisted peeling of the internal limiting membrane may cause retinal damage. Am J Ophthalmol 2001;132:431-3.

13

=

63. Sippy BD, Engelbrecht NE, Hubbard GB, et al. Indocyanine green effect on cultured human retinal pigment epithelial cells: implication for macular hole surgery. Am J Ophthalmol 2001;132:433-5.

64. Smiddy WE, Glaser BM, Thompson JT, et al. Transforming growth factor-beta 2 significantly enhances the ability to flatten the rim of subretinal fluid surrounding macular holes. Preliminary anatomic results of a multicenter prospective randomized study. Retina 1993;13:296-301.

65. Thompson JT, Smiddy WE, Williams GA, et al. Comparison of recombinant transforming growth factor-beta-2 and placebo as an adjunctive agent for macular hole surgery. Ophthalmology 1998;105:700-6.

66. Glaser BM, Michels RG, Kuppermann BD, et al. Transforming growth factor-beta 2 for the treatment of full-thickness macular holes. A prospective randomized study. Ophthalmology 1992;99:1162-73.

67. Banker AS, Freeman WR, Azen SP, Lai MY. A multicentered clinical study of serum as adjuvant therapy for surgical treatment of macular holes. Vitrectomy for Macular Hole Study Group. Arch Ophthalmol 1999;117:1499-502.

68. Kozy DW, Maberley AL. Closure of persistent macular holes with human recombinant transforming growth factor-beta 2. Can J Ophthalmol 1996;31:179-82.

69. Kusaka S, Sakagami K, Kutsuna M, Ohashi Y. Treatment of full-thickness macular holes with autologous serum. Jpn J Ophthalmol 1997;41:332-8.

70. Liggett PE, Skolik DS, Horio B, et al. Human autologous serum for the treatment of full-thickness macular holes. A preliminary study. Ophthalmology 1995;102:1071-6.

71. Melberg NS, Meredith TA. Success with macular hole surgery. Ophthalmology 1996;103:200-1.

72. Peyman GA, Daun M, Greve MD, et al. Surgical closure of macular hole using an absorbable macular plug. Int Ophthalmol 1997;21:87-91.

73. Margherio AR, Margherio RR, Hartzer M, et al. Plasmin enzyme-assisted vitrectomy in traumatic pediatric macular holes. Ophthalmology 1998;105:1617-20.

74. Trese MT, Williams GA, Hartzer MK. A new approach to stage 3 macular holes. Ophthalmology 2000;107:1607-11.

75. Vine AK, Johnson MW. Thrombin in the management of full thickness macular holes. Retina 1996;16:474-8.

76. Blumenkranz MS, Ohana E, Shaikh S, et al. Adjuvant methods in macular hole surgery: intraoperative plasma-thrombin mixture and postoperative fluid-gas exchange. Ophthalmic Surg Lasers 2001;32:198-207.

77. Thompson JT, Smiddy WE, Glaser BM, et al. Intraocular tamponade duration and success of macular hole surgery. Retina 1996;16:373-82.

78. Thompson JT, Glaser BM, Sjaarda RN, et al. Effects of intraocular bubble duration in the treatment of macular holes by vitrectomy and transforming growth factor-beta 2. Ophthalmology 1994;101:1195-200.

79. Mulhern MG, Cullinane A, Cleary PE. Visual and anatomical success with short-term macular tamponade and autologous platelet concentrate. Graefes Arch Clin Exp Ophthalmol 2000;238:577-83.

80. Goldbaum MH, McCuen BW, Hanneken AM, et al. Silicone oil tamponade to seal macular holes without position restrictions. Ophthalmology 1998;105:2140-8.

81. Pertile G, Claes C. Silicone oil vs. gas for the treatment of full-thickness macular hole. Bull Soc Belge Ophtalmol 1999;274:31-6.

14

=

82. Lai JC, Stinnett SS, McCuen BW. Comparison of silicone oil versus gas tamponade in the treatment of idiopathic full-thickness macular hole. Ophthalmology 2003;110:1170-4.

83. Tornambe PE, Poliner LS, Grote K. Macular hole surgery without face-down positioning. A pilot study. Retina 1997;17:179-85.

84. Christmas NJ, Smiddy WE, Flynn HW, Jr. Reopening of macular holes after initially successful repair. Ophthalmology 1998;105:1835-8.

85. Isomae T, Sato Y, Shimada H. Shortening the duration of prone positioning after macular hole surgery- comparison between 1-week and 1-day prone positioning. Jpn J Ophthalmol 2002;46:84-8.

86. Simcock PR, Scalia S. Phacovitrectomy without prone posture for full thickness macular holes. Br J Ophthalmol 2001;85:1316-9.

87. Leonard RE, 2nd, Smiddy WE, Flynn HW, Jr., Feuer W. Long-term visual outcomes in patients with successful macular hole surgery. Ophthalmology 1997;104:1648-52.

88. Paques M, Chastang C, Mathis A, et al. Effect of autologous platelet concentrate in surgery for idiopathic macular hole: results of a multicenter, double-masked, randomized trial. Platelets in Macular Hole Surgery Group. Ophthalmology 1999;106:932-8.

89. Kang HK, Chang AA, Beaumont PE. The macular hole: report of an Australian surgical series and meta-analysis of the literature. Clin Experiment Ophthalmol 2000;28:298-308.

90. Kobayashi H, Kobayashi K. Correlation of quantitative three-dimensional measurements of macular hole size with visual acuity after vitrectomy. Graefes Arch Clin Exp Ophthalmol 1999;237:283-8.

91. Pearce IA, Branley M, Groenewald C, et al. Visual function and patient satisfaction after macular hole surgery. Eye 1998;12 ( Pt 4):651-8.

92. Smiddy WE, Pimentel S, Williams GA. Macular hole surgery without using adjunctive additives. Ophthalmic Surg Lasers 1997;28:713-7.

93. Gaudric A, Paques M, Massin P, et al. Use of autologous platelet concentrate in macular hole surgery: report of 77 cases. Dev Ophthalmol 1997;29:30-5.

94. Polk TD, Smiddy WE, Flynn HW, Jr. Bilateral visual function after macular hole surgery. Ophthalmology 1996;103:422-6.

95. Hikichi T, Onodera A, Ishiko S, et al. Stereo acuity in patients with unilateral macular hole and after unilateral macular hole surgery. Graefes Arch Clin Exp Ophthalmol 2001;239:128-32.

96. Ezra E, Aylward WG, Gregor ZJ. Membranectomy and autologous serum for the retreatment of full-thickness macular holes. Arch Ophthalmol 1997;115:1276-80.

97. Johnson RN, McDonald HR, Schatz H, Ai E. Outpatient postoperative fluid-gas exchange after early failed vitrectomy surgery for macular hole. Ophthalmology 1997;104:2009-13.

98. Ie D, Glaser BM, Thompson JT, et al. Retreatment of full-thickness macular holes persisting after prior vitrectomy. A pilot study. Ophthalmology 1993;100:1787-93.

99. Smiddy WE, Sjaarda RN, Glaser BM, et al. Reoperation after failed macular hole surgery. Retina 1996;16:13-8.

100. Thompson JT, Sjaarda RN, Lansing MB. The results of vitreous surgery for chronic macular holes. Retina 1997;17:493-501.

101. Willis AW, Garcia-Cosio JF. Macular hole surgery. Comparison of longstanding versus recent macular holes. Ophthalmology 1996;103:1811-4.

102. Tilanus MA, Cuypers MH, Bemelmans NA, et al. Predictive value of pattern VEP, pattern ERG and hole size in macular hole surgery. Graefes Arch Clin Exp Ophthalmol 1999;237:629-35.

15

=

103. Scott RA, Ezra E, West JF, Gregor ZJ. Visual and anatomical results of surgery for long standing macular holes. Br J Ophthalmol 2000;84:150-3.

104. Ullrich S, Haritoglou C, Gass C, et al. Macular hole size as a prognostic factor in macular hole surgery. Br J Ophthalmol 2002;86:390-3.

105. Byhr E, Lindblom B. Preoperative measurements of macular hole with scanning laser ophthalmoscopy. Correlation with functional outcome. Acta Ophthalmol Scand 1998;76:579-83.

106. Ip MS, Baker BJ, Duker JS, et al. Anatomical outcomes of surgery for idiopathic macular hole as determined by optical coherence tomography. Arch Ophthalmol 2002;120:29-35.

107. Thompson JT, Sjaarda RN. Surgical treatment of macular holes with multiple recurrences. Ophthalmology 2000;107:1073-7.

108. Yamashita T, Uemara A, Uchino E, et al. Spontaneous closure of traumatic macular hole. Am J Ophthalmol 2002;133:230-5.

109. Johnson RN, McDonald HR, Lewis H, et al. Traumatic macular hole: observations, pathogenesis, and results of vitrectomy surgery. Ophthalmology 2001;108:853-7.

110. Garcia-Arumi J, Corcostegui B, Cavero L, Sararols L. The role of vitreoretinal surgery in the treatment of posttraumatic macular hole. Retina 1997;17:372-7.

111. Rubin JS, Glaser BM, Thompson JT, et al. Vitrectomy, fluid-gas exchange and transforming growth factor--beta-2 for the treatment of traumatic macular holes. Ophthalmology 1995;102:1840-5.

112. Minihan M, Goggin M, Cleary PE. Surgical management of macular holes: results using gas tamponade alone, or in combination with autologous platelet concentrate, or transforming growth factor beta 2. Br J Ophthalmol 1997;81:1073-9.

113. Thompson JT, Glaser BM, Sjaarda RN, Murphy RP. Progression of nuclear sclerosis and long-term visual results of vitrectomy with transforming growth factor beta-2 for macular holes. Am J Ophthalmol 1995;119:48-54.

114. Cheng L, Azen SP, El-Bradey MH, et al. Duration of vitrectomy and postoperative cataract in the vitrectomy for macular hole study. Am J Ophthalmol 2001;132:881-7.

115. Simcock PR, Scalia S. Phaco-vitrectomy for full-thickness macular holes. Acta Ophthalmol Scand 2000;78:684-6.

116. Lahey JM, Francis RR, Fong DS, et al. Combining phacoemulsification with vitrectomy for treatment of macular holes. Br J Ophthalmol 2002;86:876-8.

117. Paques M, Massin P, Blain P, et al. Long-term incidence of reopening of macular holes. Ophthalmology 2000;107:760-6.

118. Duker JS, Wendel R, Patel AC, Puliafito CA. Late re-opening of macular holes after initially successful treatment with vitreous surgery. Ophthalmology 1994;101:1373-8.

119. Banker AS, Freeman WR, Kim JW, et al. Vision-threatening complications of surgery for full-thickness macular holes. Vitrectomy for Macular Hole Study Group. Ophthalmology 1997;104:1442-52; discussion 52-3.

120. Park SS, Marcus DM, Duker JS, et al. Posterior segment complications after vitrectomy for macular hole. Ophthalmology 1995;102:775-81.

121. Scott IU, Moraczewski AL, Smiddy WE, et al. Long-term anatomic and visual acuity outcomes after initial anatomic success with macular hole surgery. Am J Ophthalmol 2003;135:633-40.

122. Sjaarda RN, Glaser BM, Thompson JT, et al. Distribution of iatrogenic retinal breaks in macular hole surgery. Ophthalmology 1995;102:1387-92.

16

=

123. Minihan M, Cleary PE. Autologous platelet concentrate in the surgical management of macular holes. Dev Ophthalmol 1997;29:36-43.

124. Heier JS, Topping TM, Frederick AR, Jr., et al. Visual and surgical outcomes of retinal detachment following macular hole repair. Retina 1999;19:110-5.

125. Pendergast SD, McCuen BW, 2nd. Visual field loss after macular hole surgery. Ophthalmology 1996;103:1069-77.

126. Paques M, Massin P, Santiago PY, et al. Visual field loss after vitrectomy for full-thickness macular holes. Am J Ophthalmol 1997;124:88-94.

127. Arima T, Uemura A, Otsuka S, et al. Macular hole surgery-associated peripheral visual field loss. Jpn J Ophthalmol 1998;42:476-83.

128. Boldt HC, Munden PM, Folk JC, Mehaffey MG. Visual field defects after macular hole surgery. Am J Ophthalmol 1996;122:371-81.

129. Bopp S, Lucke K, Hille U. Peripheral visual field loss after vitreous surgery for macular holes. Graefes Arch Clin Exp Ophthalmol 1997;235:362-71.

130. Welch JC. Dehydration injury as a possible cause of visual field defect after pars plana vitrectomy for macular hole. Am J Ophthalmol 1997;124:698-9.

131. Welch JC. Prevention of visual field defect after macular hole surgery by passing air used for fluid-air exchange through water. Am J Ophthalmol 1999;128:396-7.

132. Ohji M, Nao IN, Saito Y, et al. Prevention of visual field defect after macular hole surgery by passing air used for fluid-air exchange through water. Am J Ophthalmol 1999;127:62-6.

133. Gass CA, Haritoglou C, Messmer EM, et al. Peripheral visual field defects after macular hole surgery: a complication with decreasing incidence. Br J Ophthalmol 2001;85:549-51.

134. Hirata A, Yonemura N, Hasumura T, et al. Effect of infusion air pressure on visual field defects after macular hole surgery. Am J Ophthalmol 2000;130:611-6.

135. Dayan MR, Jayamanne DG, Andrews RM, Griffiths PG. Flashes and floaters as predictors of vitreoretinal pathology: is follow-up necessary for posterior vitreous detachment? Eye 1996;10:456-8.

136. Byer NE. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment. Ophthalmology 1994;101:1503-14.

137. Smiddy WE, Michels RG, de Bustros S, et al. Histopathology of tissue removed during vitrectomy for impending idiopathic macular holes. Am J Ophthalmol 1989;108:360-4.

138. American Academy of Ophthalmology. Vision Rehabilitation for Adults, Preferred Practice Pattern. San Francisco: American Academy of Ophthalmology, 2001.

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