SURVEY OF OPHTHALMOLOGY

VOLUME 37 - NUMBER 3

DIAGNOSTIC

??

November-December

19%

AND SURGICAL

TECHNIQUES

STEVEN G. KRAMER, EDITOR

Vitrectomy in the Management of Diabetic Eye Disease TONY

HO, M.D., WILLIAM

Bascom Palmer

E. SMIDDY,

Eye Institute,

M.D., AND HARRY

W. FLYNN,

University of Miami School of Medicine,

Miami,

JR,

M.D.

Florida

Abstract. Vitrectomy techniques including endolaser photocoagulation allow visual rehabilitation in many eyes that are otherwise untreatable. Discerning the indications and timing for diabetic vitrectomy is increasingly important as the treatment of complications of diabetic retinopathy continues to undergo modification and redefinition. The most common indications for diabetic vitrectomy include: 1) severe nonclearing vitreous hemorrhage; 2) traction retinal detachment recently involving the macula; 3) combined traction and rhegmatogenous detachment; 4) progressive fibrovascular proliferation; and 5) rubeosis iridis and vitreous hemorrhage for eyes in which the media opacity has prevented adequate laser photocoagulation. Other less common indications in selected cases include dense premacular hemorrhage, ghost cell glaucoma, macular edema with premacular traction, cataract preventing treatment of severe, proliferative diabetic retinopathy, anterior hyaloidal fibrovascular proliferation, and fibrinoid syndrome with retinal detachment. The rationale and surgical objectives are discussed and results are summarized. (Surv Ophthalmol37:190-202, 1992)

Key words. diabetic retinopathy fibrovascular proliferation retinal detachment vitrectomy photocoagulation ??

??

??

??

In 1967, diabetic retinopathy was described by Duke-Elder as “not preventable” and “relatively untreatable.“3g Since then, remarkable advances have been made in the management of this disease. The first therapeutic breakthrough came with the observation that coexisting chorioretinal scars seemed to provide a protective effect against the development of proliferative disease.’ The application of this observation was to mimic the same effect iatrogenically with extensive laser photocoagulation of the peripheral retina. Subsequently, the efficacy of panretinal laser photocoagulation in limiting the progression of proliferative diabetic

retinopathy and reducing the incidence of severe visual loss was proven.29-g3 Laser photocoagulation was later applied for diabetic macular edema,9~l1,19,25,49,46,57,66,66,69,80,92,99, 105~‘og~11’~“3 and definitively proven effective in reducing the risk of moderate visual loss due to clinically significant diabetic macular edema.40 Some eyes develop progressive proliferative complications despite prompt and appropriate laser treatment. Others present with severe proliferative complications for which laser treatment cannot be applied. Vitrectomy may be beneficial in these eyes.

190

VITRECTOMY

191

IN MANAGEMENT OF DIABETIC EYE DISEASE

A Brief History of Vitrectomy Therapeutic vitrectomy has a relatively short history. The concept of removing the vitreous gel to treat blinding conditions was introduced in 1962 with the observations of Kasner who used planned “open-sky vitrectomy” to successfully rehabilitate many eyes with severe vitreous opacities.52*53 In 1970 Machemer pioneered the concept of pars plana vitrectomy using a “closed eye” system and “automated” vitrectomy.62p65 Development in techniques and advances in microinstrumentation followed. Vitrectomy was initially used in diabetic cases with severe nonclearing vitreous hemorrhage, and later applied to cases with retinal detachment associated with vitreoretinal tractional membranes, restoring vision for many eyes with extremely poor prognosis. Its usefulness has been extended to many other vitreoretinal diseases including giant retinal tears, penetrating proliferative vitreoretinopathy and injuries, macular diseases.

Indications for Vitrectomy in Diabetic Eye Disease The indications for vitrectomy in diabetic retinopathy have been expanded and refined over the past decade. The earliest indications were severe nonclearing vitreous hemorrhage for 6 to 12 months, tractional retinal detachment recently involving the macula, and combined tractional and rhegmatogenous retinal detachment.1,2,4’,54, 64~74~82~g3~1’ The 5efficacy of early vitrectomy to remove vitreous hemorrhage and allow timely laser treatment in eyes with rubeosis iridis, and surgery for rapidly progressive fibrovascular proliferation involving the macula was also recognized. “,‘l Overall, the rate of visual improvement in cases of diabetic vitrectomy has remained about 67%.“,lo3 This apparent lack of increased success is probably attributable to the changing distribution of indications, with a higher proportion of more complex cases being attempted. A review of a series of diabetic vitrectomies in 1977 found 70% were for nonresolving vitreous hemorrhages, 20% were for tractional macular detachments, and 10% for combined tractional and rhegmatogenous detachments.* By 1987 the distribution of indications included only about 15-25% solely for nonresolving vittractional macular dereous hemorrhages, tachments (3040%), combined tractional and rhegmatogenous detachments (17-35%), and progressive severe fibrovascular proliferation

(IO-12%).4J03 Further indications have been recognized with increased experience and understanding of the pathophysiology of advanced diabetic retinopathy (Table 1). These include dense premacular hemorrhage, 77,85~103 g host cell glaucoma,g7 macular edema with premacular hyaloid traction5’ and cataract with severe proliferative diabetic retinopathy. 10,‘7,55Two newer indications for reoperation have been identified in eyes following diabetic vitrectomy - anterior hyaloidal fibrovascular proliferation5”“’ and librinoid syndrome associated with retinal detachment.‘j*“’ Preoperative factors indicating a poorer postoperative prognosis regardless of the indication include: preoperative iris neovascularization, cataract, visual acuity >5/200, and retinal deThese factors play a major role in tachment. 13~100 determining the timing and suitability of vitrectomy. Once a stable anatomic and visual result has been obtained, it remains stable longterm in a large majority of cases. ‘8,84The rationale, surgical objectives, and results for each of these indications are reviewed below. SEVERE NONCLEARING HEMORRHAGE

VITREOUS

Vitreous hemorrhage from retinal new vessels is a frequent complication of proliferative diabetic retinopathy. Usually this is mild and self-limiting, and in the absence of other complicating factors such as retinal detachment or severe fibrovascular proliferation, a conservative approach is adopted. Panretinal laser photocoagulation is utilized first in an attempt to stabilize or achieve regression of the proliferative retinopathy. The krypton laser and the more recently introduced diode systems may allow treatment through moderate vitreous hemorrhage, since red and infrared wavelengths are transmitted through hemoglobin pigments better than the blue and green wavelengths of the argon.47 Also, laser indirect ophthalmoscopic delivery systems allow treatment when significant central or posterior hemorrhage blocks slit-lamp laser delivo the vitreous hemorrhage is dense ery. 48~1’When enough to prevent adequate laser treatment and spontaneous clearing does not occur, vitrectomy is considered. Historically, vitrectomy was reserved for cases in which the vitreous hemorrhage persisted for at least six months. The Diabetic Retinopathy Vitrectomy Study (DRVS) demonstrated that early vitrectomy (14 months after onset of severe vitreous hemorrhage causing 5/200 vision)

192

Surv Ophthalmol

37 (3) November-December TABLE

1992

HOETAL

1

Cuwent Indications for Vitrectomyin Diabetic Eye Disease 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Severe nonclearing vitreous hemorrhage Tractional retinal detachments recently involving the macula Combined tractional and rhegmatogenous retinal detachments Severe progressive fibrovascular proliferation Anterior segment neovascularization with posterior segment opacity Dense premacular hemorrhage Ghost cell glaucoma Macula edema associated with premacular traction Cataract preventing treatment of severe proliferative diabetic retinopathy Anterior hyaloidal fibrovascular proliferation 11. Fibrinoid syndrome with associated retinal detachment

resulted achieving

in a slightly higher

proportion

a final vision of r20/40.s5,38

of cases A final vi-

sion of 2 20/40 was attained in 25% of cases in the early vitrectomy group, but in only 15% of cases in the group in which vitrectomy was deferred either 12 months or until macular detachment occurred (p = 0.1). The difference was more marked for the subgroup of patients with Type I (juvenile-onset, insulin-dependent) diabetes (36% vs. 12%, p = O.OOl), indicating that the optimal timing of vitrectomy for severe vitreous hemorrhage in Type I diabetics is sooner, around three months after onset. The proportion losing light perception at 24 months’ followup was not statistically different in the early vitrectomy group (25%) compared with the conventional management group (1 9%).35 The better results in Type I cases are probably related to the tendency for Type I diabetic patients to have more extensive new vessels, fibrous proliferations, and vitreoretinal adhesions. Therefore, they were at greater risk for complications such as retinal detachment and progressive fibrovascular proliferation while waiting for the vitreous hemorrhage to clear. It is notable that these results were obtained without the benefit of laser endophotocoagulation, which was not available until the mid 1980s.29*44S56,7g Thus, the recommended timing of vitrectomy is generally about six months after acute hemorrhage for Type II patients, but after only about three months for Type I cases. These general guidelines may be modified depending upon the known extent and activity of Iibrovascular proliferation, posterior vitreous detachment, extent of prior laser treatment, status of the fellow eye, and other medical conditions which may require priority treatment before surgery is contemplated (such as severe hypertension). Echographic

monitoring of the posterior retina is recommended to detect the need for earlier intervention if progressive retinal detachment is observed. The surgical goals are to remove the vitreous hemorrhage and to provide a clear media, application of laser photocoagulation, and removal of anterior to posterior vitreous traction on fibrovascular fronds, decreasing the potential for further growth and hemorrhage. Previously, photocoagulation treatment was given postoperatively, but modern endolaser systems now permit intraoperative photocoagulation.23~44~56~7g This allows immediate, convenient, and thorough laser panretinal photocoagulation on the operating table. Successful results with improved vision have been reported in 59-83% of cases.13~35~38~63~84~83~100~103 The rate of postoperative vitreous hemorrhage has been decreased with the use of endolaser photocoagulation. Vitreous hemorrhage following vitrectomy is a common finding, but is usually self-limited and clears spontaneously. In about 10% of cases with postoperative hemorrhage, spontaneous clearing does not occur and further surgery should be considered.76 This may be performed in the operating room using three-port pars plana incisions, or as an outpatient, office procedure involving fluid-gas exchange.‘4,74 If vitreous hemorrhage is the sole cause of decreased vision, the results are good, but if further proliferative complications have ensued, vision is limited accordingly. TRACTIONAL RETINAL DETACHMENT INVOLVING THE MACULA Tractional retinal detachment involving the macula is currently the most common indication for diabetic vitrectomy. 4,103Extraretinal fibrovas-

VITRECTOMY

IN MANAGEMENT OF DIABETIC EYE DISEASE

193

Fig. 1. Z&: A 54-year-old black diabetic female developed progressive tractional retinal detachment involving the macula of the right eye in association with foci offibrovascular proliferation along the mid-portion of the inferotemporal arcade and the distal portion of the superotemporal arcade. Vision decreased to 20/200. The patient underwent vitrectomy, membrane dissection, and endolaser photocoagulation. Right: The vision two years following surgery remains 20/30. There’s no macular traction and the fbrovascular stumps are atrophic.

cular tissue grows within the vitreous just anterior to its posterior surface.45 Contraction of the proliferative tissues causes the variably separated cortical vitreous to exert anteroposterior vitreoretinal traction between the vitreous base and posterior fibrovascular tissues attached to the retina. There may also be tangential traction between one posterior vitreoretinal adhesion and another. As a result, the complexity of the vitreoretinal detachment can vary widely. Vitrectomy is considered when the macula has been detached only within the previous several months. Vitrectomy is not usually performed in eyes with extramacular traction detachments since the incidence of progression to involve the macula is only about 15% per year, whereas reported failure rates for diabetic eyes subject to vitrectomy are much higher.24 However, in some patients with clearly progressive tractional detachment, the macula is threatened, and early vitrectomy may allow a better chance to achieve the surgical objectives, preserving optimal longterm vision.36,37,78 Macular detachment for more than six months usually precludes the return of useful vision. Chronic retinal detachment is accompanied by thinner, more atrophic retina and more extensive, tightly adherent fibrovascular membranes. The prognosis is poorer in cases with macular detachment > 6 months, extensive detachment, vitreous hemorrhage, lack of preoperative and severe neovascularizaphotocoagulation, tion 3~13~15~51~82~89~101~103~106

The surgical objectives include removal and relief of media opacities, anteroposterior and tangential tractional elements by excision of posterior vitreous, and preretinal fibrovascular membranes’5,73 (Fig. 1). The areas of elevated retina often reattach after major tractional elements are relieved without need for transvitreal drainage of subretinal fluid and gas tamponade. Other surgical objectives include attention to hemostasis and closure of iatrogenic breaks by laser photocoagulation and internal gas tamponade. Anatomic success as judged by reattachment of the macula has been reported to be from 65% to 80% (6 months minimum follow-up) and improved visual acuities from 26% to 65%. 3,5,73,75,82,89,101,103 COMBINED TRACTIONAL AND RHEGMATOGENOUS RETINAL DETACHMENT Combined traction and rhegmatogenous retinal detachment occurs when the fibrovascular traction is severe enough to create a retinal break. Visual loss occurs more suddenly and profoundly than with traction macular detachment. The retinal break is usually located posterior to the equator, adjacent to areas of fibrovascular proliferation. The break is often small and may occur within areas of previous laser treatment. Therefore, they may be difficult to find, even with slit-lamp biomicroscopy. However, clinical features are characteristic (Fig. 2). Most notable is the mobile appearance with hydration

194

Surv Ophthalmol

37 (3) November-December

1992

HOETAL

Fig. 2. Z_& In cases with combined diabetic retinal detachment, the retinal hole may not be immediately evident, but the clinical appearance is characteristic, with inner retinal white lines indicating the hydration lines of any rhegmatogenous detachment, mobile retina, and more widespread extent of retinal detachment compared to tractional detachments. Right: The retinal break is usually present posterior to the equator, as seen here in the temporal midperiphery of a patient with combined traction and rhegmatogenous retinal detachment.

lines. Hydration lines are seen as white lines in the inner retina and are diagnostic of rhegmatogenous detachment. The retinal detachment rapidly becomes more extensive and the inner retinal surface has a convex configuration. Conventional scleral buckling methods alone are usually not successful because of persistent vitreoretinal traction and posterior location of the retinal break. The indication for surgery is the sudden loss of vision in association with the rhegmatogenous retinal detachment. Preoperative factors associated with a better postoperative prognosis include preoperative vision >5/200, absence of rubeosis iridis, and absence of macular detachment.g0’102 The surgical objectives are relief of traction and identification and treatment of retinal breaks (Fig. 3). Posterior vitreous and preretinal fibrovascular membranes are dissected and excised to relieve anteroposterior and tangential tractional elements. Subretinal fluid is evacuated transvitreally during fluid-gas exchange, flattening the retina to allow treatment of the break with endolaser photocoagulation or transvitreal retinocryopexy. Temporary intraocular gas tamponade is used while the permanent chorioretinal adhesion occurs. Scleral buckling may be considered when peripheral breaks are encountered or if traction cannot be completely relieved. Posterior breaks do not require buckling,

although it is important to relieve traction. Lensectomy may be indicated in cases complicated by proliferative vitreoretinopathy (PVR) or recurrent retinal detachments, particularly when there is anterior fibrovascular proliferation. Visual acuity improves in about one-half of patients and vision of 51200 or better has been obtained in 55_62%.8%%9’&ion In selected cases complicated by severe PVR and recurrent retinal detachments, silicone oil tamponade may be indicated to provide prolonged tamponade.41’67*g1”14 Silicone oil is rarely indicated in a primary diabetic vitrectomy. SEVERE PROGRESSIVE PROLIFERATION

FIBROVASCULAR

Progressive growth of active fibrovascular tissue may occur despite extensive photocoagulation treatment. Typically this occurs in a young, Type I diabetic who often has suboptimal control of serum glucose. The Iibrovascular proliferation occurs quickly and posterior vitreous detachment is not present. These eyes rapidly progress to severe visual loss.34,36 The results of conventional treatment (vitrectomy only after one year of nonclearing vitreous hemorrhage or traction macular detachment) allowed study of the natural history of 744 eyes with severe proliferative diabetic retinopathy in Group N of the Diabetic Retinopathy Vitrectomy Study (DRVS).34 With conventional, nonsurgical

EYE DISEASE

195

left:This 45-year-old diabetic female had been initially seen with early nonmacular tractional retinal detachment and vision of 20/30. Despite panretinal photocoagulation, traction increased. Finally, there was a precipitous loss of vision to 3/200. The appearance of hydration lines most prominently superior to the macula indicates combined traction and rhegmatogenous retinal detachment extending into the center of the macula. Top tight: The fibrovascular proliferation was most marked superonasal to the optic nerve head. This was the region of the hole, although it was not evidenced preoperatively. Bottom left:Postoperatively, the traction is relieved in the retina and the macula reattached with return of vision to 20/40. Bottom right: The preoperative hole is flat and its edges are sealed with a laser-induced chorioretinal adhesion. Fig. 3. Top

management, visual loss was more frequent during the first year of follow-up than during the second, and was related to baseline visual acuity level and severity of the fibrovascular proliferation. After two years, vision was less than 5/200 in 45% of eyes with 20/60-2OllOO visual acuity at baseline and more than 4 disc areas of new vessels versus 14% of eyes without active new vessels, or fresh vitreous hemorrhage at baseline and with extramacular tractional detachments. Vitrectomy was eventually performed in 25% of cases, but only when severe vitreous hemorrhage failed to clear over 12 months, or if macular traction detachment occurred. The

results

of Group

N justified

study of an

NR group in a second part of the DRVS. The NR group included 370 eyes with severe fibrovascular proliferation and vision ~20/400 that were randomly assigned to either early vitrectomy or conventional management (as described above).36 The percentage of eyes with a visual acuity of 20140 or better was 44% in the early vitrectomy group and 28% in the conventional management group after four years of follow-up (p < 0.05). The proportion with very poor visual outcome was similar in the two groups. These results indicate that early vitrectomy should be considered in eyes with advanced fibrovascular proliferation that progresses despite photocoagulation, even if useful vision is still retained. Pre-

196

Surv Ophthalmol

37 (3) November-December

1992

HOETAL

Fig. 4. left: A 20-year-old diabetic male presented with a two-month history of decreased vision in the right eye. Visual acuity measured 20/400. Panretinal photocoagulation was initiated, but the visual acuity remained in the 20/400 range. Thereis marked, progressive fibrovascular proliferation with a subhyaloid hemorrhage covering the macula despite prompt PRP. Right: Vitrectomy was performed with peeling of the fibrovascular tissue and supplemental endolaser photocoagulation. Vision improved to 20/40 six months postoperatively. Although there is residual epiretinal membrane, the macular traction of the fibrovascular tissue has been removed, relieving a majority of the macular traction. The fellow eye followed a similar course, requiring laser and vitrectomy.

Fig. 5. Left:A 35-year-old diabetic female presented with macular traction secondary to extensive fibrous proliferation in the right eye. Visual acuity was 31200 and no preexisting posterior vitreous separation was noted. Right: Vitrectomy with membrane peeling, and endolaser photogoagulation were performed. The vision remained 20/50 two years postoperatively.

operative factors indicating a more favorable postoperative result include age 540 years, preoperative vision ~5/200, absence of iris neovascularization, and preoperative photocoagulation.28 The surgical objectives are to remove the posterior vitreous surface en bloc with the fibrovascular tissue and to apply endolaser panretinal photocoagulation to arrest the proliferative proces? (Fig. 4). Intraoperative bleeding limits

achievement of the surgical objectives. Intraocular diathermy, increased infusion pressure and intravitreal thrombin may be helpful in achievis more easily ing hemostasis. 27~104Hemostasis achieved in cases with more chronic (and hence less vascular) fibrovascular proliferation (Fig. 5). Vision improved in 70% of eyes following surgery for progressive fibrovascular proliferation, and 82% regained vision ~5/200.~~ The fibrovascular

tissue

can be more

completely

removed

VITRECTOMY

IN MANAGEMENT OF DIABETIC EYE DISEASE

197

Fig. 6. Left: A 4%year-old diabetic male presented with dense, premacular hemorrhage in the left eye, decreasing vision to 34/200. Right: Postoperatively, visual acuity improved to 20140 and the subhyaloid hemorrhage has been evacuated.

with early intervention, before substantial areas of tissue anchor into the retina. This is the rationale for early surgery, but surgery should not be considered to obviate the need for maximal preoperative laser treatment.

ANTERIOR SEGMENT NEOVASCULARIZATION SEGMENT OPACITY

WITH

POSTERIOR

Anterior segment neovascularization with posterior segment opacity presents within a spectrum ranging from mild rubeosis to severe neovascular glaucoma. New vessels in the anterior segment probably arise secondary to posterior segment ischemia. The iris new vessels may cause progressive angle closure and marked elevation of intraocular pressures. Early treatment is the key to avoiding severe neovascular glaucoma.]” Vitrectomy has two possible roles to play in the management of this clinical problem. The first is in cases with progressive rubeosis and posterior segment opacities that prevent adequate prophylactic panretinal photocoagulation treatment. Cases with mild, nonprogressive rubeosis iridis may be safely observed, but when moderate rubeosis is progressing and vitreous hemorrhage prevents panretinal photocoagulation, surgery should be considered. In these cases the surgical objective is to clear the media and deliver panretinal endolaser photocoagulation to induce regression of the new vessels and preservation of good vision. ” Results depend upon the severity of posterior segment ischemia and its response to photocoagulation. The second role of vitrectomy is in cases with

established neovascular glaucoma where extensive angle neovascularization renders medical therapy and conventional filtering procedures unsuccessful. The surgical objective in such cases is to lower intraocular pressure by combining pars plana vitrectomy (usually with lensectomy and endolaser) with a filtration procedureg6 or Molten0 filtration implant.6’ The Molten0 implant method appears to have higher success rates as defined by intraocular pressures of less than 26 mm Hg (70% versus 50%) and loss of light perception (14% versus 20%).6’,g6 Staging the procedure by initial ligature of the tubes avoids hypotony and lessens the risk of sterile fibrinous vitritis and suprachroidal hemorrhage. 61 Visual results are disappointing. DENSE PRE-MACULAR

HEMORRHAGE

Subhyaloid hemorrhage occurs in an area of neovascularization without preexisting vitreous detachment. Most will clear spontaneously or following panretinal photocoagulation, often by developing breakthrough vitreous hemorrhage, and surgery will not be necessary. However, a subgroup of patients present with extensive, dense, nonclearing subhyaloid hemorrhage confined within an incomplete posterior vitreous detachment overlying the macula. Untreated, the internal limiting membrane or posterior cortical hyaloid can serve as both a scaffold for fibrovascular proliferation, subsequent traction macular detachment, or fovea1 ectopia from epiretinal membrane contracture.77’85”03 Vitrectomy is considered if panretinal photocoagulation does not induce involution of the

198

Surv Ophthalmol

37 (3) November-December

proliferative retinopathy and the dense hemorrhage remains confined in the premacular space for several months. Early vitrectomy is also considered if visual rehabilitation has been delayed due to persistent subhyaloid blood. The surgical objectives include removing the posterior hyaloid, evacuating the hemorrhage and, if necessary, completing the panretinal photocoagulation (Fig. 6). Performing surgery within a couple months allows surgical dissection more readily since a plane of dissection is already established, resulting in better visual results and lower complication rates.77’s5 Surgical success rates in such cases are about 85%. Cases operated on later may require more extensive membrane peeling and segmentation. GHOST CELL GLAUCOMA Marked elevation of intraocular pressures may occur in eyes with vitreous hemorrhage.” This characteristically occurs in aphakic eyes with a disrupted anterior hyaloid face or following vitrectomy, while waiting for the vitreous hemorThe pressure rise occurs rhage to clear.“~4g~50~‘08 due to impedance of outflow in the trabecular meshwork from degenerated red blood cells (ghost cell glaucoma). ” The erythroclastic cells are less pliable and are spherical, thus cannot be as readily cleared as normal red blood cells. The resulting glaucoma usually lasts for months. The indication for surgery is uncontrolled intraocular pressure despite maximal medical therapy. However, since the pressure rise may be selflimited, intraocular pressures in the mid-30s can be tolerated for a few weeks before surgical intervention. This entity should be distinguished from increased intraocular pressure rise due to corticosteroid responsiveness, which resolves upon discontinuing the drops. The surgical objective is to remove the source of erythroclastic cells by removing the vitreous blood. A series of three cases of ghost cell glaucoma was reported with normalization of intraocular pressure following pars plana vitrectomy and anterior chamber washout.g7 MACULAR EDEMA ASSOCIATED PREMACULAR TRACTION

WITH

Severe, diffuse, laser-resistant macular edema may be secondary to premacular traction from the attached posterior hyaloid.58 The vitreoretinal interface shows a characteristic wrinkling due to an attached and thickened posterior hya-

1992

HOETAL

loid. These cases are uncommon and distinct from the usual macular edema. Visual acuity may improve after vitrectomy with removal of the posterior hyaloid and epiretinal membranes. Surgery may be indicated when vision has decreased to the level of 20/80 or worse, since the approach and management of such cases parallels that for other causes of macular pucker. The surgical objective is to excise the thickened posterior hyaloid, relieving surface traction. Initial results following vitrectomy have been encouraging, but require further study.58 CATARACT PREVENTING TREATMENT SEVERE PROLIFERATIVE DIABETIC RETINOPATHY

OF

In addition to causing poor vision, a cataract may prevent satisfactory monitoring or adequate panretinal laser photocoagulation of severe proliferative diabetic retinopathy. Lens opacities only rarely prohibit laser treatment, since krypton red laser can be used to penetrate nuclear is recomsclerotic opacities. Photocoagulation mendable for proliferative disease before cataract surgery, but in rare cases the cataract surgery must be performed first to allow sufficiently clear media for panretinal photocoagulation. Contemporary techniques in wound closure have allowed laser photocoagulation treatment soon after the cataract surgery. Rapid progression of neovascular proliferation and neovascular glaucoma following both intracapsular and extracapsular cataract extraction have been documented.8vs4 Rarely, patients will present with dense cataract and severe complications of proliferative retinopathy, necessitating vitrectomy. Lens opacities can be diflicult to assess accurately when the vitreous cavity contains a large hemorrhage, and there is no benefit in achieving surgical results of diabetic vitrectomy with lens removal.” Thus, a two-step approach is usually the management of choice. In certain situations a one-step combined procedure of cataract extraction, lens implantation, pars plana vitrectomy and panretinal endolaser photocoagulation offers the advantages of visual rehabilitation with a single operation in a shorter time. This approach may be indicated for patients who are nonambulatory or have problems with transportation, or for those whose medical ailments preclude convenient slit-lamp delivery of panretinal laser or cause increased risk of medical complications even with surgery under local anesthesia.

VITREXTOMY IN MANAGEMENT OF DIABETIC EYE DISEASE The surgical objectives include management of the cataract and posterior segment complications by a combined procedure. This may be achieved by performing a standard extracapsular cataract extraction (ECCE) or phacoemulsification with posterior chamber intraocular lens (PC/IOL) implantation followed by a pars plana vitrectomy and endolaser.” An alternative is to do a pars plana lensectomy, leaving intact the anterior lens capsule, followed by pars plana vitrectomy, endolaser, and insertion of the PC/IOL in front of the anterior lens capsule. A central anterior capsulotomy is then performed.17,55 Although a higher rate of rubeosis in aphakic eyes was documented in early series of diabetic vitrectomy,‘6*88,g4 the availability of endolaser photocoagulation may be the reason for a lower incidence in combined series.‘7*55 Postoperative rubeosis iridis has not been a problem following combined procedures. Hence, combined lensectomy and diabetic vitrectomy is now safer. Furthermore, visual rehabilitation of aphakic eyes is more problematic in diabetics, so IOL is preferred. The visual and anatomic results in such patients are encouraging.‘0~‘7~55

ANTERIOR HYALOIDAL PROLIFERATION

FIBROVASCULAR

Progressive anterior hyaloidal fibrovascular proliferation (AIIFVP) is a severe complication occurring after vitrectomy for diabetic retinopathy that occurs in 13% eyes followed for an average of 12 months. 5g Patients tend to be young with extensive retinal neovascularization and severe retinal ischemia. The proliferation starts in the anterior peripheral retina or vitreous base region and extends to the equator and posterior surface of the lens. Subsequent contraction causes peripheral traction retinal detachment, pulling the peripheral retina anteriorly and centrally towards the lens, resembling anterior loop contraction seen in eyes with proliferative vitreoretinopathy (PVR). The fibrous tissue is avascular in PVR, but is highly vascular in AHFVP. AHFVP occurs more frequently in cases with traction retinal detachment as the indication for surgery, placement of a scleral buckle, postoperative rubeosis iridis, recurrent vitreous hemorrhages, or multiple surgeries.5g Treatment of AHFVP is difficult and often unsuccessful. If it is detected in an early, mild stage, additional anterior panretinal photocoagulation may be effective in controlling the process. Surgical indica-

199

tions are poorly defined, but repeat surgery is considered in cases with evident retrolenticular membranes that are increasing in size within the first several weeks following initial surgery. Surgical objectives include removal of the anterior tissue and stabilization of the proliferative process. Most advanced cases require scleral bucking, lensectomy, resection of the anterior and peripheral vitreous including membrane dissection, and extensive and confluent laser or retinocryopexy treatment to the peripheral retina and pars plana. Extensive retinotomy with silicone oil may be necessary to achieve retinal reattachment. In a series of eight such patients, four responded favorably to extensive additional photocoagulation or additional vitreous surgery.5g

FIBRINOID SYNDROME ASSOCIATED WITH POSTVITRECTOMY RETINAL DETACHMENT Massive postoperative intravitreal fibrin may complicate vitreous surgery in diabetic eyes.g5 Probably this represents the severe end of a spectrum of postoperative fibrin formation in the vitreous cavity. More frequently, mild fibrin forms in the anterior chamber. When this is mild, intracamera1 tissue plasminogen activator is effective in dissolving the fibrin clot.26,“2 Fibrin formation is most common and severe when extensive vascular membrane dissection, lensectomy, scleral buckling procedure or extensive endolaser panretinal photocoagulation have been performed with vitrectomy. Interlacing fibrin strands form on the retinal surface and at the iris plane within the first few postoperative hours. In the fibrinoid syndrome, a gelatinous mass of tissue forms in the center of the vitreous cavity, leading to tractional retinal detachment and rubeosis iridis with neovascular glaucoma. The typical patient with the fibrinoid syndrome is a young diabetic with rapidly progressive diabetic retinopathy, often with poor medical control, renal complications, loss of antithrombolysin III in the urine, and abnormalities in the coagulation cascade.“sg8 Corticosteroids (systemic, topical, periocular, and intraocular), intraocular tissue plasminogen activator,12’ and streptokinase26 are effective in mild cases, but the prognosis in severe cases is poor. Repeat vitrectomy is usually unsuccessful. Preoperative systemic corticosteroid treatment theoretically blocks the release of arachnidonic acid at the capillary site, but such theoretical therapy is yet unproven by adequate clinical trials.6

200

Surv Ophthalmol 37 (3) November-December

Conclusion A better understanding of the pathobiology of proliferative diabetic retinopathy emphasizing prompt, aggressive laser photocoagulation treatment has preserved useful vision in a high proportion of cases. In addition, recent advances in vitrectomy techniques and instrumentation have enabled successful visual rehabilitation in many severely affected eyes which would have previously been blind. The remarkable progress made toward the management of a disease that was described as “unpreventable” and “untreatable” only two decades ago, emphasizes the urgent goal of the Diabetes 2000 Project” to eliminate preventable diabetes-related blindness by the year 2000. The key strategy to achieving this is continuing education of the medical community and establishment of mechanisms for prompt referral and treatment.

References 1. Aaberg TM: Results of 100 consecutive vitrectomy procedures, in McPherson A (ed): Controversial Aspects of Vitreoretinal Surgery. St Louis, CV Mosby, 1977, pp 245-249 2. Aaberg TM: Vitrectomy for diabetic retinopathy, in Freeman HM, Hirose T, Schepens CL (eds): Vitreous Surgery and Advances in Fundus Diagnosis and Treatment. New York, Appleton-Century-Crofts, 1977, pp 297-313 3. Aaberg TM: Pars plana vitrectomy for diabetic traction retinal detachment. Ophthalmology 88:639-642, 1981 4. Aaberg TM, Abrams GW: Changing indications and techniques for vitrectomy in management of complications of diabetic retinopathy. Ophthalmology 94:775779, 1987 5. Aaberg TM, Van Horn DL: Late complications of pars plana vitreous surgery. Ophthalmology 85:126-140, 1978 6. Aaberg TM, Williams GA: Pharmacology of surgery of the vitreous and retina, in Sears ML, Tarkkanen A (eds): Surgical Pharmacologyof the Eye. New York, Raven Press, 1985, pp 503-528 7. Aiello LM, Beetham WP, Balodimos MC, et al: Ruby laser photocoagulation in treatment of diabetic proliferating retinopathy: preliminary report, in Goldberg ML and Fine SL (eds): Symposium on the Treatment of Diabetic Retinopathy, US Public Health Service Publication no. 1890. Washington DC, US Government Printing Office, 1968 8. Aiello RC, Wand M, Liang G: Neovasculara glaucoma and vitreous hemorrhage following cataract surgery in patients with diabetes mellitus. Ophthalmology 90:814-

820, 1983 9. Behrendt T: Therapeutic vascular occlusions in diabetic retinopathy. Arch Ophthalmol 87:629-633, 1972 10. Benson WE, Brown GC, Tasman W, McNamara JA: Extracapsular cataract extraction, posterior chamber lens insertion, and pars plana vitrectomy in one operation. Ophthalmology 97:819-921, 1990 11. Blankenship GW: Diabetic macular edema and laser photocoagulation. Ophthalmology 86:69-75, 1979 12. Blankenship GW: The lens influence on diabetic vitrectomy results. Report of a prospective randomized

1992

HOETAL,

study. Arch Ophthalmol 98:219&2198, 1980 13. Blankenship GW: Preoperative prognostic factors in diabetic pars plana vitrectomy. Ophthalmology89: 12461249, 1982 14. Blankenship GW: Management of vitreous cavity hemorrhage following pars plana vitrectomy of diabetic retinopathy. Ophthalmology 93:39-44, 1986 15. Blankenship GW: Proliferative diabetic retinopathy: Principles and techniques of surgical treatment, in Ryan SJ (ed), Retina. St Louis, CV Mosby, 1989, pp 515-539 16. Blankenship GW, Cortez R, Machemer R: The lens and part plana vitrectomy for diabetic retinopathy complications. Arch Ophthulmol 97:1263-1267, 1979 17. Blankenship GW, Flynn HW Jr, Kokame G: Posterior chamber intraocular lens insertion during pars plana lensectomy and vitrectomy for complications of proliferative diabetic retinopathy. Am J Ophthalmol 108:1-5, 1989 18. Blankenship GW, Machemer R: Longterm diabetic vitrectomy results. Report of a IO-year-follow-up. Ophthalmology 92:503-506, 1985 19. British Multicentre Study Group: Photocoagulation for diabetic maculopathy: A randomized controlled clinical trial using xenon arc. Diabetes 32:1010-1016, 1983 20. Brownlee M, Vlassara H, Cerami A: Inhibition of heparin-catalyzed human antithrombin III activity by nonenzymatic glycosylation; possible role in fibrin deposition in diabetes. Diabetes 33:532-535, 1984 21. Campbell DGG, Simmons RJ, Tolentino FI, McMeel JW: Glaucoma occurring after closed vitrectomy. Am J Ophthalmol83:63-69, 1977 22. Campbell DG, Simmons RJ, Grant WM: Ghost cells as a cause of glaucoma. Am J Ophthalmol81:441-450, 1976 23. Charles S: Endophotocoagulation. Retina 1: 117-120, 1981 24. Charles S, Flinn CE: The natural history of diabetic extramacular traction retinal detachment. Arch Ophthalmol99:66-68, 198 1 25. Cheng G, Blach RD, Hamilton AM, et al: Diabetic maculopathy. Trans Ophthalmol Sot UK 92:407-411, 1972 26. Cherfan GM, Maghraby AE, Tabbara KF, et al: Dissolution of intraocular fibrinous exudate by streptokinase. Ophthulmology 98:87Q-874, 199 1 27. De Bustros S, Glaser BM, Johnson MA. Thrombon infusion for the control of intraocular bleeding during vitreous surgery. Arch Ophthalmol 103:837-839, 1985 28. De Bustros S, Thompson JT, Michels RG, Rice TA: Vitrectomy for progressive proliferative diabetic retinopathy. Arch Ophthalmol 105:196-199, 1987 29. Diabetic Retinopathy Study Research Group: Preliminary report on effects of photocoagulation therapy. Am J Ophthalmol81:383-396, 1976 30. Diabetic Retinopathy Study Research Group: Photocoagulation treatment of proliferative diabetic retinopathy: The second report of Diabetic Retinopathy Study findings. Ophthalmology 85:82-106, 1978 31. Diabetic Retinopathy Study Research Group: Four risk factors for severe visual loss in diabetic retinopathy. Arch Ophthalmol 97:654-655, 1979 32. Diabetic Retinopathy Study Research Group: Photocoagulation treatment of proliferative diabetic retinopathy: Relationship of adverse treatment effects to retinopathy severity. Diabetic Retinopathy Study Report No 5. Dev Ophthalmol 2:248-261, 1981 33. Diabetic Retinopathy Study Research Group: Photocoagulation treatment of proliferative diabetic retinopathy: Clinical application of Diabetic Retinopathy Study (DRS) Findings, DRS Report No. 8. Ophthalmology 88:583-600, 1981 34. Diabetic Retinopathy Vitrectomy Study Research Group: Two-year course of visual acuity in severe proliferative diabetic retinopathy with conventional management. DRVS Report No 1. Ophthalmology 92:492-

201 502, 1985 35. Diabetic Retinopathy Vitrectomy Study Research Group: Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy: Two-year results of randomized trial. DRVS Report No 2. Arch Ophthalmol 103:1644-1652, 1985 36. Diabetic Retinopathy Vitrectomy Study Research Group: Early vitrectomy for severe proliferative diabetic retinopathy in eyes with useful vision: Results of a randomized trial. DRVS Report No 3. Ophthalmology 95:1307-1320, 1988 37. Diabetic Retinopathy Vitrectomy Study Research Group: Early vitrectomy for severe proliferative diabetic retinopathy in eyes with useful vision. Clinical application of results of a randomized trial. DRVS Report No 1988 4. Ophthalmology 95:1321-1334, 38. Diabetic Retinopathy Vitrectomy Study Group: Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy. Four-year results of a randomized trial: DRVS Report No. 5. Arch Ophthalmol 108:958-964, 1990 39. Duke-Elder S: System of Ophthalmology, Vol 10. St Louis, CV Moshy, 1967, pp 10 40. Early Treatment Diabetic Retinopathy Study Research Group: Photocoagulation for diabetic macular edema. ETDRS Report no 1. Arch Ophthalmol 103: 1796-l 806, 1985 41. Ehud A, Varda C, Joseph M, Giora T: Management of complicated retinal detachment by vitrectomy and silicone oil injection. Metabol Pediatr System Ophthalmol 1988 11:63-66, 42. Eifrig D, Lockhart DL, Berglund RD, Knobloch WH: Pars plana vitrectomy Oflhthul Surg 9:76-88, 1978 43. Ferris FL, Patz A: Macular edema: A complication of diabetic retinopathy. Sun, Ophthalmol28:452461, 1984 44. Fleischman JA, Swartz M, Dixon JA: Argon laser endophotocoagulation, an intraoperative trans-pars plana technique. Arch Ophthalmol 99:1610-1612, 1981 45. Foos RY, Kreiger AE, Nofsinger K: Pathologic study following vitrectomy for proliferative diabetic retinopathy. Retina 5:101-106, 1985 46. Foulds WS: The role of photocoaguiation in the treatment of retinal disease. Trans Ophthalmol Sot NZ 32: 92-90, 1980 47. Fanfois J, Cambie E: Retinal photocoagulation (xenonarc and lasers). Ann Ophthalmol3:1201-1208, 1979 48. Friberg TR: Clinical experience with a binocular indirect ophthalmoscope laser delivery system. Retina 7: 28-31, 1987 49. Ghartey KN, Tolentino FI, Freeman HM, et al: Closed vitreous surgery. XVII. Results and complications of pars plana vitrectomy. Arch Ophthalmol 98: 1248-1252, 1980 50. Han DP, Lewis H, Lambrou FH, Jr, et al: Mechanisms of intraocular pressure elevation after pars plana vitrectomy. Ophthalmology 96:1357-1362, 1989 51. Hutton WL, Bernstein I, Fuller DG: Diabetic traction 1980 retinal detachment. Ophthalmology 87:1071-1077, 52. Kasner D: Vitrectomy: A new approach to the management of vitreous. Highlights in Ophthalmology 11:304329, 1969 53. Kasner D: The technique ofradical anterior vitrectomy in vitreous loss, in Welsh RC, Welsh J (eds): The New Report on Cataract Surgery. Miami, Miami Educational Press, 1969, pp. l-4 54. Kloti R: Indications for vitrectomy and results in 115 cases, in McPherson A (ed): Controversial Aspects of Vitreoretinal Surgery. St Louis, CV Mosby, 1977, pp 237-244 55. Kokame GT, Flynn HW Jr, Blankenship GW: Posterior chamber intraocular lens implantation during diabetic pars plana vitrectomy. Ophthalmology 96:603-610, 1989 56. Landers MB III, Trese MT, Stefansson E, Bessler M: Argon laser intraocular photocoagulation. Oflhthalmol-

OQ 89:785-788, 1982 57. L’Esperance FA: The treatment of ophthalmic vascular disease by argon laser photocoagulation. Ophthalmology 72:1077, 1096, 1968 58. Lewis H, Abrams GW, Blumenkranz MS, Campo RV: Resolution of diabetic macular edema associated with a thickened and taut premacular posterior hyaloid after vitrecotomy (abstract). Oflhthalmology 98 (Suppl):146, 1991 59. Lewis H, Abrams GW, Williams GA: Anterior hyaloidal fihrovascular proliferation after diabetic vitrectomy. Am J Oflhthalmol104:607-613, 1987 60. Liggett PE, Lean JS, Barlow WE, Ryan SJ: Intraoperative argon endophotocoagulation for recurrent vitreous hemorrhage after vitrectomy for diabetic retinopathy. Am J Ophthulmol 103:146-149, 1987 61. Lloyd MA, Heuer DK, Baerveldt G, et al: Combined Molten0 implantation and pars plana vitrectomy for neovascular glaucoma. Ophthulmology 98:1401-1405, 1991 62. Machemer R, Buettner H, Norton EWD, Pare1 JM: Vitrectomy: A pars plana approach. Trans Am Acad Ophthulmol Otolaryngol 72:4 104 18, 1968 63. Machemer R, Hickingbotham D: The three-port microcannular system for closed vitrectomy. Am J Ophthalmol 100:590-592, 1985 64. Machemer R, Norton EWD: A new concept for vitreous surgery. 3. Indications and results. Am J Ophthalmol 74:1034-1055, 1972 65. Machemer R, Pare1 JM, Buettner H: A new concept for vitreous surgery. I. Instrumentation. Am J Ophthalnwl 73:1-7, 1972 66. Marcus DG, Aaberg TM: Argon laser photocoagulation treatment in diabetic cystoid maculopathy. Ann Ophthalmol 9:365-372, 1977 67. McCuen BW II, Rinkoff JS: Silicone oil for progressive anterior ocular neovascularization after failed diabetic vitrectomy. Arch Ophthalnwl 107:677-682, 1989 68. McMeel JW, Trempe CL, Franks EB: Diabetic maculopathy. Ophthalmol 83:476487, 1977 69. Merin S, Yanko L, Ivry M: Treatment of diabetic maculopathy by argon laser. Br J Ophthalmol58:85-91, 1974 70. Michels RG: Vitreous Surgery. St Louis, CV Mosby, 1981, pp 215-216 71. Michels RG: Vitrectomy for complications of diabetic retinopathy. Arch Ophtkulmol 96:237-246, 1978 72. Michels RG, Ryan SJ Jr: Results and complications of 100 consecutive cases of pars plana vitrectomy. Am J Ophthalmol 80:24-29, 1975 73. Miller SA, Butler JB, Myers FL, Bresnick GH: Pars Plana vitrectomy. Treatment for tractional macula detachment secondary to proliferative diabetic retinopathy. Arch Ophthalmol 98:659-664, 1980 74. Miller JA, Chandra SR, Stevens TS: A modified technique of performing outpatient fluid-air exchange following vitrectomy surgery. Am J Ophthulmol 101:116117, 1986 75. Nakae R, Saito Y, Nishikawa N, Ikeda T, Tano Y: Results of vitrectomy for diabetic traction retinal detachment involving the macula: a comparison of six-month and three-year post-operative findings. Nippon Ganka Gakkai Zasshi-Acta Societatis Ophthalmologicae Japonica 93:271-275, 1989 76. Novak MA, Rice TA, Michels RG, Auer C: Vitreous hemorrhage after vitrectomy for diabetic retinopathy. Ophthalmology 91:1485-1489, 1984 77. O’Hanley GP, Canny CLB: Diabetic dense pre-macular hemorrhage: a possible indication for prompt vitrectomy. Ofihthalmology 92:507-511, 1985 78. Packer AJ: Vitrectomy for progressive macular traction associated with proliferative diabetic retinopathy. Arch Ophthalmol 105:1679-1683, 1987 79. Parke DW III, Aaberg TM: Intraocular argon laser

202

80.

81. 82.

83.

84.

85.

86.

87.

88.

89.

90.

91.

92. 93.

94.

95.

96.

97. 98.

Surv Ophthalmol 37 (3) November-December photocoagulation in the management of severe proliferative vitreoretinopathy. Am J Ophthulmol97:434-443, 1984 Patz A, Schatz H, Berkow JW, et al: Macular edema: An overlooked complication of diabetic retinopathy. Ophthulmol 77:34-%2, I973 Patz A, Smith RE: The ETDRS and Diabetes 2000. Ophthalmology 98:739-740, 199 1 Peyman GA, Huamonte FU, Goldberg MF, et al: Fourhundred consecutive pars plana vitrectomies with the vitrophage. Arch Ophtbdmol 96:45-50, 1978 Peyman GA, Raichand M, Huamonte FU, et al: Vitrectomy in 125 eyes with diabetic vitreous haemorrhage. Br J Ophthalmd 60:752-755, 1976 Pollack A, Dotan S, Oliver M: Progression of diabetic retinopathy after cataract extraction. Br J Ophthulmol 75:547-551, 1991 Ramsay RC, Knobloch WH, Cantrill HL: Timing of vitrectomy for active proliferative diabetic retinopathy. Ophthalmology 93:283-289, 1986 Ratner CM, Michels RG, Auer C, Rice TA: Pars plana vitrectomy for complicated retinal detachments. Ophthalmdogy 90:1323-1327, 1983 Rice TA, Michels RG: Long-term anatomic and functional results of vitrectomy for diabetic retinopathy. Am J Ophthalmol90:297-303, 1980 Rice TA, Michels RG, Maguire MG, Rice EF: The effect of lensectomy on the incidence of iris neovascularization and neovascular glaucoma after vitrectomy for diabetic retinopathy. Am J Ophthulmol 95: l-1 1, 1983 Rice TA, Michels RG, Rice EF: Vitrectomy for diabetic traction retinal detachment involving the macula. Am J 1983 Ophthalmol95:22-23, Rice TA, Michels RG, Rice EF: Vitrectomy for diabetic rhegmatogenous retinal detachment. Am J Ophthdmol 95~34-44, 1983 Rinkoff JS, de Juan E Jr, McCuen BW: Silicone oil for retinal detachment with advanced proliferative vitreoretinopathy following failed vitrectomy for proliferative diabetic retinopathy. Am J Ophthulmol 101: 18 l-l 86, 1986 Rubinstein K, Myska V: Treatment of diabetic maculopathy. Br J Ophthalmol 56~1-5, 1972 Ryan SJ, Michels RG: Pars plana vitrectomy, indications and results in 100 cases, in McPherson A (ed): Controversial Aspects of Vitreoretinal Surgery. St Louis, CV Mosby, 1977, pp 250-256 Schachat AP, Oyakawa RT, Michels RG, Rice TA: Complications of vitreous surgery for diabetic retinopathy. II. Postoperative complications. Ophthalmology 90:522530, 1983 Sebestyen JG: Fibroinoid syndrome: a severe complication of vitrectomy in diabetics. Ann Ophthalmol 14: 853-856, 1982 Sinclair HS, Aaberg TM, Meredith TA: A pars plana filtering procedure combined with lensectomy and vitrectomy for neovascular glaucoma. Am J Ophtbdmol 93:185-191, 1982 Singh H, Grand MG: Treatment ofblood-induced glaucoma by tram plana vitrectomy. Retina 1:255, 1981 Sowers JR, Tuck ML, Sowers DK: Plasma antithrombin III and thrombin generation time: correlation with he-

1992

99.

100.

101.

102.

103.

104.

105.

106.

107.

108.

109.

110.

111.

112.

113.

114.

115.

HOETAL moglobin Al and fasting serum glucose in young diabetic women. Diabetes Care 3:665-668, 1980 Spalter H: Photocoagulation of circinate maculopathy in diabetic retinopathy. Am J Ophthulmol 71:242-250, 1971 Thompson JT, Auer CL, deBustros S, et al: Prognostic indicators of success and failure in vitrectomy for diabetic retinopathy. Ophthulmology 93:290-295, 1986 Thompson JT, de Bustros S, Michels RG, Rice TA: Results and prognostic factors in vitrectomy for diabetic traction retinal detachment ofthe macula. Arch Ophthulmol 105:497-502, 1987 Thompson JT, de Bustros S, MIchels RG, Rice TA: Results and prognostic factors in vitrectomy for diabetic traction-rhegmatogenous retinal detachment. Arch Ophthulmol 105:503-507, 1987 Thompson JT, de Bustros S, Michels RG, et al: Results of vitrectomy for proliferative diabetic retinopathy. Ophthalmology 93:1571-1574, 1986 Thompson JT, Glaser BM, Michels RG, de Bustros S: The use of intravitreal thrombin to control hemorrhage during vitrectomy. Ophthulmulogy 93:279-282, 1986 Ticho U, Patz A: The role of capillary perfusion in the management of diabetic macular edema. Am J Ophthalmol 76:880-886, 1973 Tolentino FI, Freeman HM, Tolentino FL: Closed vitrectomy in the management of diabetic traction retinal detachment. Ophthalmology 87:1078-1089, 1980 Wand M: Neovascular glaucoma, in Ritch R, Shields MB, Krupin T (eds): The Glaucomas. St Louis, CV Mosby, 1989, pp 323-325 Weinberg RS, Peyman GA, Huamonte FU: Elevation of intraocular pressure after pars plana vitrectomy. Albrecht von Graefes Arch Klin Exp Ophthalmol200: 157-161, 1976 Wetzig PC, Worlton JT: Treatment of diabetic retinopathy by light-coagulation. Br J Ophthulmol47:539-544, 1963 Whitacre MM, Manoukian N, Mainster MA: Argon indirect ophthalmoscopic photocoagulation: reduced potential phototoxicity with a fixed safety filter. Br J Ophthalmol 74:233-234, 1990 Whitelocke RAF, Kearns M, Blach RK, et al: The diabetic maculopathies. Trans Ophthalmol Sot UK 99:314320, 1979 Williams GA, Lambrou FH, Jaffe GA, et al: Treatment of post-vitrectomy fibrin formation with intraocular tissue plasminogen activator. Arch Ophthulmol 106: 10551058, 1988 Wiznia RA: Photocoagulation of non-proliferative exudative diabetic retinopathy. Am J Ophthulmol88:22-27, 1979 Yeo JH, Glaser BM, Michels RG: Silicone oil in the treatment of complicated retinal detachments. Ophthulmology 94:1109-1113, 1987 Young PW, Shea M: Pars plana vitrectomy. Can J Ophthalmol 12:106-I 13, 1977

Reprint address: William 016880, Miami FL 33101.

E.

Smiddy,

M.D.,

PO Box