|SYMPOSIUM - DIABETIC RETINOPATHY UPDATE
|Year : 2014 | Volume
| Issue : 1 | Page : 41-54
The surgical management of diabetic retinopathy complications: An update
Hazem A El-Sabagh
Department of Ophthalmology, Vitreoretinal Unit, Magrabi Eye and Ear Center, Dammam, Saudi Arabia
|Date of Web Publication||3-Mar-2015|
Dr. Hazem A El-Sabagh
Vitreoretinal Unit, Magrabi Eye and Ear Center, P. O. Box 1840, Dammam 31441
Source of Support: None, Conflict of Interest: None
Diabetic complications are known to be one of the leading causes of visual loss in the working age group in the developed world. The vitreous plays an important role in the development and progression of proliferative diabetic retinopathy and its complications. Despite the proper management of diabetics, complications due to disease progression necessitating diabetic vitrectomy occurs at a rate of 0.2% of people with diabetes. Vitrectomy has been used for the management of the complications of proliferative diabetic retinopathy since 1970, since then, the continuing developments in instrumentations and techniques have greatly improved outcome and minimized complications. This article reviews the updates in vitrectomy for the management of diabetic retinopathy, including indications, outcome, instrumentations, techniques and complications. The Medline database was searched for all literatures using the words, proliferative diabetic retinopathy, vitrectomy, diabetic macular edema, and vitreolysis.
Keywords: Diabetic macular edema, proliferative diabetic retinopathy, vitrectomy, vitreolysis
|How to cite this article:|
El-Sabagh HA. The surgical management of diabetic retinopathy complications: An update. Egypt Retina J 2014;2:41-54
| Introduction|| |
Although diabetic complications are known to be one of the leading causes of visual loss in the working age group in the developed world,  yet, the problem is even worse in the developing countries due to poor management of diabetic patient. ,
Structural abnormalities of the retinal vessels as well as complex biochemichal abnormalities occurring in the eyes of diabetics result in diabetic retinopathy, ,, which is classified into nonproliferative and proliferative. Nonproliferative diabetic retinopathy is apparent clinically as intraretinal hemorrhages, retinal edema, and lipid exudates. The hallmark of proliferative diabetic retinopathy (PDR) is neovascularization. 
The role of the vitreous in the development and progression of PDR has been described.  It was suggested that the vitreous cortex seems to be involved in early stages of the diabetic disease, whereas the vitreous gel influences the late stages. ,,, Moreover, the precocious liquefaction and syneresis in the vitreous of diabetics leads to anomalous posterior vitreous detachment (PVD) that exerts traction on the newly formed vessels lifting them from the retinal surface into the vitreous cavity. ,
Later on as the disease progresses, anteroposterior traction exerted by the shrinking vitreous body  and/or the tangential one by the contracting epiretinal fibrovascular proliferations (EFVP), in the presence of tight vitreoretinal adhesions will eventually lead to vitreous hemorrhage (VH) or tractional complications including; retinoschisis, tractional retinal detachment (TRD), and formation of retinal breaks resulting in combined tractional rhegmatogenous retinal detachment (TRRD). Moreover, traction on the macula either by thickened posterior vitreous face or by contracting EFVP may lead to diabetic macular edema, macular distortion, macular heterotopia,  or may produce partial or full-thickness macular holes by traction on thin ischemic fovea. 
Despite the proper management of diabetics, complications due to disease progression necessitating diabetic vitrectomy occurs at a rate of 3.7% at 5 years in patients with significant diabetic retinopathy  or 0.2% of people with diabetes, in general. 
This article reviews the updates in vitrectomy for the management of diabetic retinopathy, including indications, outcome, instrumentations, techniques, and complications.
| Management of the Complications of Diabetic Retinopathy|| |
Indications for surgery
Pars plana vitrectomy was first reserved to severe, nonclearing VH. Since then, refinement in instrumentation and techniques, as well as the increasingly reported favorable outcome of vitrectomy led to extension of the indications for pars plana vitrectomy and a lowered threshold for surgical intervention. 
In acute VH, blood may be present in the vitreous gel and/or in the subhyaloid space. Subretinal hemorrhage is a rare type in association with long-term, advanced PDR that carries a guarded visual prognosis, and may indicate the presence of a retinal break. 
When bleeding occurs into the vitreous cavity, the amount and location of hemorrhage predict how fast it is going to clear spontaneously. Although visual acuity improvement can occur few months after VH in a good number of patients, however, a larger number end up with poor visual outcome which could be due to persistent VH, or development or progression of TRD, as well as development of red cell or neovascular glaucoma (NVG). ,,,
Type of diabetes and duration of VH were the main factors influencing the decision to operate on a dense nonclearing VH based on Diabetic Retinopathy Vitrectomy Study (DRVS) results that outlined the benefits of early rather than delayed vitrectomy in patients with Type 1 diabetes for eyes with severe VH and severe visual loss, while no such advantage was found in the Type 2 diabetes group.  Since then, it is increasingly accepted to observe patients with Type 1 diabetes presenting with dense non clearing VH for 1 month, and longer for those with Type 2 diabetes.  However, regardless of the duration of VH, some patients and certain types of pathologies necessitate earlier surgical intervention as in patients with bilateral severe VH, VH in a monocular patient, the presence of rubeosis iridis or RD and in patients with preexisting severe fibrovascular proliferations or untreated diabetic maculopathy.  Furthermore, patients with no prior pan retinal photocoagulation are at great risk of development of neovascular complications and must be watched more closely.  Moreover, few reports have described rapid progression of dense pre-macular subhyaloid hemorrhages to TRD, with consequent poor visual outcome, hence, earlier intervention may be considered in these cases. , It is worth mentioning that a nonrecordable flash visual evoked cortical potentials in a diabetic eye with severe VH does not necessarily mean an inoperable case and should be perceived cautiously. 
Other nonsurgical intervention for vitreous hemorrhage
Nonsurgical interventions for the management of VH have been described, including neodymium-doped yttrium aluminum garnet posterior hyaloidotomy, ,,, and intravitreal anti-vascular endothelial growth factor (VEGF) injection, , However, the limited number of reported cases and the lack of randomized prospective studies, as well as the possible side-effects of blood in the vitreous cavity, or the reported development or progression of TRD shortly after intravitreal injection of bevacizumab,  makes these treatment modalities short of being used routinely, and rather reserved for some selected patients.
| Severe Fibrovascular Proliferations and Tractional Complications|| |
Hutton et al. described five common configurations of TRD based on the extent of vitreoretinal attachment, as well as height and location of RD  [Figure 1]. TRD is currently the main indication for vitrectomy in diabetic patients. , However, since extramacular TRD can be quite stable,  patients with extramacular TRD are usually suitable candidate for observation. The rate of progression of extramacular TRD to involve the macula was 13.8% at 1 year, 21% at 2 years, and 23% at 3 years.  The general advice to patients with this type of TRD is to seek immediate medical attention if they noticed visual deterioration, otherwise, patients with extramacular TRD can be followed-up at 3 months intervals.
|Figure 1: Different configurations of traction retinal detachment (TRD). (a) Hammock-shaped TRD, (b) central diffuse TRD|
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Whilst TRD with recent onset macular involvement is a well-established indication for vitrectomy, ,, surgery for traction RD threatening the macula is increasingly practiced now-a-days. This indication for vitrectomy, however, is still controversial with some surgeons preferring to operate only on cases that have symptomatic changes in vision due to macular involvement. 
Other indications for vitrectomy surgery include combined traction and RRD and progressive EFVP. In patients with progressive EFVP, favorable outcomes were observed in the early vitrectomy group, where rate of final visual acuity of 20/40 or better was 44% compared with 28% in the conventional management group. , Fewer complications are expected during removal of EFVP when the zone of vitreoretinal attachments is less extensive, extends less anteriorly and is more acute (having less tenacious adhesions). 
Surgery for diabetic macular edema
Vitreous gel has been suggested to play a role in the pathogenesis of diabetic macular edema. , Lewis et al.  first reported vitrectomy to remove thickened taut posterior hyaloid (TTPH) in association with impaired vision and diabetic macular edema. Their findings have been further substantiated after the invention of optical coherence tomography, which demonstrated evident vitreomacular traction in some patients with diabetic macular edema  [Figure 2]. Resolution of macular edema and visual improvement have been reported after vitrectomy in patients with tractional diabetic macular edema. , However, the role of vitrectomy for diabetic macular edema without TTPH has been controversial, ,,, and it is unclear if there is any benefit of performing internal limiting membrane peeling in these cases. ,, In the absence of randomized controlled trials, vitrectomy for nontractional diabetic macular edema has currently been superseded by the rapidly evolving pharmacotherapy developments, including intravitreal corticosteroids and anti-VEGF drugs. ,,
|Figure 2: Vitreomacular traction caused by thickened taut posterior hyaloid leading to severe macular edema|
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| Instrumentation|| |
Since the introduction of vitrectomy in 1970's,  several advances in vitreoretinal instrumentation have greatly expanded the spectrum of indications, changed the surgical techniques, and improved the visual outcome achieved. Improved visualization with better illumination and viewing systems and more efficient vitrectomy machines with versatile vitrectomy cutters, are the main benefits of recent advances in vitreoretinal instrumentation.
Wide-angle viewing systems provide better peripheral retinal visualization during epiretinal membrane removal, with less creation and early detection of retinal breaks and consequently reduced the incidence of postoperative RD. , However, due to its less axial (depth) resolution, one should pay attention when working close to the retina or lens to avoid unintended trauma.  Flat irrigating contact lenses (Machemer) are preferable for epiretinal membrane dissection.
Fiberoptic Xenon illumination offers a brighter illumination that is advantageous especially with small gauge endoilluminators. Furthermore, different illuminated multifunction instruments as well as the use of chandelier illumination allow for a bimanual dissection of epiretinal membranes [Figure 3].
| Small Gauge Vitrectomy|| |
Since the introduction of 25-gauge sutureless transconjunctival vitrectomy in 2002, there is growing interest in the use of small gauge vitrectomy systems for various vitreoretinal indications.  Increased flexibility of small probes, a drawback limiting the use of earlier 25-gauge vitrectomy system for complex PDR cases, has been significantly eliminated in the newer generation of probes, which are 57% stiffer.  Lower suction and flow rates were considered by some as a drawback; however, they have been described to offer a greater fluidic stability. At high-speeds cutting offered by these systems, there is a port-based flow limiting, which greatly reduces fluid surge and iatrogenic retinal break formation, this, in addition to the shorter port to tip distance in these probes that make cutter delamination feasible and safe  [Figure 4]. The lately introduced 23-gauge vitrectomy system is described to have the same advantages of 25-gauge while offering stiffer instruments that allow more complete anterior vitrectomy, better fluidics due increased flow rates with the slightly larger diameter of the probe. This allows greater aspiration rates for inducing vitreous detachment and more efficient core vitrectomy. , Newer vitrectomy systems are using dual pneumatic cutters in which the use of springs to open the cutter port (which limits the flow rate at high speed cutting due to fixed spring recoil) has been replaced by employing air jets to open and close the ports, allowing a port open/port closed ratio of 50% even at 5000 cuts/min. 
|Figure 4: High speed 23-gauge vitreous cutter used for delamination of a proliferative membrane over a detached retina|
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| Surgical Techniques|| |
Careful planning is the key to success in vitreoretinal surgery in general and diabetic vitrectomy in particular. Good knowledge of the surgical anatomy and pathophysiologic mechanisms of the complications of PDR are pivotal in setting the surgical goals in order to achieve anatomical as well as functional success.
Although several techniques have been described for treating TRD, surgical goals remain the same; to clear media opacity, to relieve traction on the retinal surface and reattach the retina, to halt disease progression, and to prevent complications. 
Key steps in diabetic vitrectomy
Posterior hyaloid separation
Whether the VH is associated with EFVP or not, posterior hyaloid separation is a crucial step in diabetic vitrectomy. However, in the presence of EFVP its timing may differ according to the surgical strategy adopted. In the absence of EFVP, If the posterior hyaloids is completely attached, the central vitreous is removed first with the cutter, followed by active suction with the vitrector or soft-tipped extrusion cannula over the optic nerve head to elevate the posterior hyaloid face, which can then be incised with the cutter and an edge followed out to the periphery circumferentially. 
If the elevation of the posterior hyaloid failed after attempted active suction, incision of the posterior hyaloid over the nasal mid periphery with a bent needle, or elevation of the Weiss ring with a forceps or a hook can be used to detach the posterior hyaloids. 
In general, It is not necessary to remove the extreme anterior periphery of the vitreous since manipulation of the vitreous base could lead to a retinal dialysis.  However, in the presence of VH involving the anterior vitreous, peripheral gel should be removed as much as possible to avoid hemorrhage into the vitreous cavity and red cell glaucoma caused by blood leaching postoperatively.  Minimizing creation of retinal tears during vitreous shaving can be achieved by scleral indentation which help stabilize the retina, as well as the use of less port opening in the new vitrectomy machines with duty cycle control.
| Surgery for Severe Fibrovascular Proliferation and Tractional Complications|| |
On dealing with EFVP and their tractional complications, there are three basic surgical strategies; segmentation, delamination, and en bloc delamination. Each of these strategies aim at achieving the previously set surgical goals; however, they differ in the order of achieving them. While segmentation and delamination relieve anteroposterior traction forces first then deal with the tangential forces afterwards the en bloc delamination technique and its modifications deal with the tangential forces first in the presence of the anteroposterior traction which will eventually be released later on. Peeling, on the other hand is rarely resorted to for the removal of EFVP due to the inherent risk of creating retinal tears in the presence of strong vitreoretinal attachments at photocoagulation scars and between the epiretinal proliferations and the retina at the epicenters. However, it can be used for removal of taut posterior hyaloid or internal limiting membrane removal off the macular surface for the management of tractional diabetic macular edema.
Although each surgeon usually prefers a specific technique, however, sometimes the complexity of the case necessitates applying more than one technique to have a difficult case successfully completed.
| Segmentation and Delamination Techniques|| |
After truncation of the posterior vitreous cortex circumferentially to release all the anteroposterior traction forces, we are left with a skirt of posterior vitreous cortex adherent to the EFVP in a complex that can be located above the retinal surface or adherent to the retina. The membrane is adherent to the retina at single or multiple points, these points of vitreoretinal adherences are then identified and severed using either segmentation and/or delamination.
In segmentation, relief of tangential traction is achieved by cutting of the bridging fibrovascular and cortical vitreous membranes between vascular epicenters using manual or automated vertical scissors, , curved scissors,  after applying diathermy to EFVP to avoid bleeding [Figure 5]. After completion of segmentation, all the posterior tangential traction is relieved, and we end up with multiple stumps of fibrovascular membranes that were originally described to undergo involution.  Now-a-days, after the initial scissor segmentation of membranes, the remaining islands of fibrovascular membranes are trimmed using vitreous cutter, or excised using horizontal scissors. Segmentation is especially effective in areas of atrophic retina, which may tear using other techniques. 
|Figure 5: Delamination. While exerting gentle traction on the epiretinal fibrovascular proliferations using fiberoptic diathermy tissue manipulator, curved scissors are used to cut its points of attachment to the retina|
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In delamination, relief of tangential traction is achieved by introducing the tip of a horizontal scissor under cleavage planes, transecting the direct attachment between the fibrovascular membranes and the retina. This allows the removal of epiretinal membranes at the retinal plane in one or more large pieces. , this is thought to minimize bleeding from remaining fibrovascular epicenters, or the possible tear obscuration or creation by their subsequent contraction. Recently, small gauge vitrectomy cutters has been used for fibrovascular membrane delamination. 
Since cutting with the scissor tips beneath an opaque membrane leads to poor visibility, and due to uneven topography of the retinal surface, creation of retinal holes or transection of vessels are common complications.  Bimanual technique using a chandelier light or a multifunction instrument (lighted picks, lighted forceps, or the fiberoptic diathermy tissue manipulator),  is used to slightly stretch the epiretinal membrane to expose the plane of dissection and identify epicentres [Figure 5]. Residual fibrovascular stalk at the optic nerve head can be left, but its removal ensures complete relief of peripapillary traction. 
It is noteworthy that if the cleavage plane between posterior hyaloid-fibrovascular membrane complex and the retina is hard to find, the correct plane can be found by starting in the macular area followed by dissecting outwards towards the arcades. 
En block technique
In the en block technique, the posterior hyaloid is left totally or partially intact, exerting anteroposterior traction on the posterior attachments to the fibrovascular membrane to elevate and immobilize the edge of the membrane during dissection. As the tangential traction is released, the anteroposterior traction exerted by the posterior hyaloid will consequently be relieved and then the vitreous cutter is used to remove all the separated posterior hyaloid and membranes. ,, While the en bloc technique facilitates the complete removal of epiretinal membranes and minimizes the complications associating residual fibrovascular stumps; however, the disadvantages of this techniques are the greater risk of retinal breaks during epiretinal membrane dissection, or from traction on the vitreous base. 
| Combined Tractional and Rhegmatogenous Retinal Detachment|| |
Combined TRD and RRD cases are considered to be of major complexity. The presence of elevated mobile retina due to the RRD increases the difficulty encountered during epiretinal membrane dissection. Bimanual dissection techniques are of great value, providing safer dissection and less creation of retinal tears. Successful retinal reattachment depends on finding the causative retinal tear, releasing all traction around it, applying endolaser photocoagulation to its edges after flattening the retina under air or using perfluorocarbon liquid, and then applying an appropriate internal retinal tamponade.  The retinal break usually occurs posterior to the equator, with common sites being at the base of vitreoretinal adhesions, or areas adjacent to previous chorioretinal scars. Adjunctive surgical techniques have been resorted to in complex cases to make surgery easier, like the perfluorocarbon-perfused pars plana vitrectomy, , hydroseparation of the posterior vitreous cortex,  or the viscodissection of epiretinal membranes. 
| Intraocular Tamponade|| |
Intraocular tamponade is required in many cases undergoing vitrectomy. Simple retinal breaks can be managed successfully by performing fluid-gas exchange. The shorter acting SF6 gas is preferred than the longer acting C3F8 due to the possibility of fibrin formation around the long-term bubble in diabetic RD. , Early breakdown of blood-retinal barrier in diabetic eyes could be contributing to this. 
Silicon oil may be used when there are multiple retinal breaks or a large retinectomy, in the presence of iris neovascularization and in repeat surgery for postdiabetic vitrectomy complications. Silicon oil is also ideal for monocular patients to allow for early visual rehabilitation.  Silicon oil with higher viscosity of 5000 centistokes (cs) is preferred than the lower viscosity one (1000 cs) as an endotamponade in 20-gauge vitrectomy surgery due to its higher stability, while a recently introduced lower viscosity silicon oil, that offers better stability than the 1000 cs silicon oil combined with easier surgical handling than the higher viscosity 5000 cs one could be a viable option for small gauge vitrectomy systems.(Siluron 2000© and Siluron ® Xtra, Fluoron, Neu-Ulm, Germany). ,,
| Special Considerations in Diabetics|| |
Ischemic nature of the disease
Due to the ischemic nature of the disease, postoperative pressure spikes were found to be a risk factor for compromising visual outcome in the vulnerable ischemic diabetic retina.  Moreover, VEGF elaborated from ischemic retinal tissues faces different barriers during its diffusion into the anterior segment to exit the eye through the trabecular meshwork. Hence, the presence or absence of vitreous, vitreous substitutes, lens or lens capsule determine the site of VEGF accumulation and the subsequent neovascularization that could include preretinal, anterior hyaloidal fibrovascular proliferation (AHFVP), as well as iris or trabecular meshwork neovascularization.  Every effort should therefore be made to eliminate the upregulation of VEGF production from ischemic retina by sufficient panretinal photocoagulation. ,,,
Vitreoschisis is a split in the posterior vitreous cortex that results as a consequence of anomalous PVD.  Vitreoschisis has been described with high incidence in patients with PDR. , Intraoperative recognition of vitreoschisis is important as the correct surgical cleavage plane for dissection is under the posterior leaf of the split posterior vitreous cortex. Accessing this plane makes dissection easier and safer. Intravitreal triamcinolone acetonide has been used to visualize residual cortical vitreous intraoperatively which if left might promote postoperative reproliferation [Figure 6]. 
|Figure 6: Posterior vitreoschisis with significant traction exerted on the retina close to the point where the two layers of the split posterior vitreous cortex re-join into one full thickness layer. The correct surgical cleavage plane is under the posterior leaf of the split posterior vitreous cortex (arrow)|
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Diabetes as a procoagulant state
During diabetic vitrectomy, it is well-noticed that bleeding on the retinal surface readily clots forming an adherent sheet, which if left or if postoperative bleeding occurs may lead to dense epiretinal proliferation [Figure 7].  Intravitreal heparin infusion has been used intraoperatively to help remove clotting preretinal hemorrhage. 
|Figure 7: (a) Dense preretinal bleeding under silicon oil occurring after diabetic vitrectomy, (b) organized blood clot ended up forming dense fibrovascular proliferation|
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| Management of the Lens in Diabetic Vitrectomy|| |
Combining phacoemulsification and intraocular lens implantation with pars plana vitrectomy has its advocates.  Better peroperative visualization, the tendency for more preoperative lens opacities in diabetics compared with other patients in the same age group, the rapid progression of cataract after vitrectomy, and the longer visual rehabilitation with sequential surgical approach are good arguments for combining both procedures.  The use of intraoperative panretinal photocoagulation reduced the previously reported increased incidence of iris neovascularization and NVG. ,
However, sequential vitrecomy and cataract surgery avoid some of the reported intraoperative disadvantages of combined surgery such as corneal wound dehiscence due to globe manipulation during vitrectomy, pupillary miosis, loss of corneal transparency, prismatic effect and undesired light reflections with early lens implantation before starting vitrectomy, and decenteration or capture of intraocular lens with gas or silicon oil tamponade, or postoperative complications like severe anterior chamber inflammatory reaction and fibrinous response. 
In summary, both, combined and sequential procedures have been found to be effective and safe. , However, combined surgery is not recommended for severe ischemic eyes, with severe TRD, or iris neovascularization complicating advanced PDR where a severe fibrinous inflammatory reaction is expected. 
| Pharmacologic Vitreolysis|| |
Pharmacologic vitreolysis is a recent growing field of interest for the management of different vitreoretinal pathologies with several agents being investigated; including hyaluronidase, tissue plasminogen activator (tPA), plasmin and microplasmin.
Purified ovine hyaluronidase (Vitrase, ISTA Pharmaceuticals, Inc., CA, USA) has been investigated for its efficacy and safety in the management of VH. It produces vitreous liquefaction that may facilitate rapid clearance of VH enough to allow for PRP and possibly obviate vitrectomy in some cases. Moreover, its preoperative use increases the rapidity of vitreous removal, , similar observations have been reported with plasmin use for the management of EFVP in PDR,  as well as the reported PVD induction following intravitreal tPA use.  Microplasmin is another pharmacologic agent under investigation that has been shown to increase the likelihood of induction and progression of PVD after a single intravitreal injection of 125 μg 1 week before surgery, which may facilitate vitrectomy, and in some cases may obviate the need for surgery. 
| Postoperative Complications|| |
The complications of diabetic vitrectomy has been reported nearly 30 years ago,  Since then, refinement of techniques and improvements in vitrectomy instruments have led to lowered incidence of surgical complications. Recurrent VH, neovascular complications, and RRD are the principal complications of pars plana vitrectomy in diabetic patients.
| Vitreous Hemorrhage|| |
In the early postoperative period, some amount of VH has been reported in 75% of eyes following diabetic vitrectomy. Postoperative vitreous cavity hemorrhage usually clears rapidly over a period of few to several weeks. However, delayed recurrent vitreous cavity hemorrhage has been reported in nearly one-third of the patients.  Most self-limited VHs probably result from clot lysis of cut ends of dissected fibrovascular tissue,  especially with postoperative hypotony.  Persistent or recurrent vitreous cavity hemorrhage could be caused by fibrovascular ingrowth at sclerotomy sites, insufficient retinal photocoagulation, residual or recurrent neovascular membrane on the optic nerve, residual and recurrent epiretinal proliferative membrane, retinal vein occlusion, and ocular trauma. ,,, In one study, postoperative VH occurred in 32% of patients undergoing 23-gauge vitrectomy for PDR.  Park et al. did not find a significant difference in the incidence of postoperative VH when comparing 20- and 23-gauge vitrectomy systems for PDR cases,  while in other series, postoperative VH occurred only in 7.5% and 11.8% of cases undergoing 23- and 25-gauge vitrectomy for PDR, respectively. ,
Careful dissection of EFVP with complete hemostasis is an important preventive measure.  Peripheral retinal treatment by cryotherapy or near confluent laser has been advocated to reduce postoperative VH. , Preoperative intravitreal anti-VEGF therapy with bevacizumab has been reported to provide some benefits; , however, in a recent study, intraoperative bevacizumab injection failed to prevent re-bleeding in eyes undergoing pars plana vitrectomy for treatment of diabetic VH, probably because of the short half-life of bevacizumab. 
| Retinal Tears and Rhegmatogenous Retinal Detachment|| |
Secondary RD complicating intraoperative iatrogenic retinal breaks remains the most common sight-threatening complication of vitrectomy. Retinal breaks are usually peripheral,  and less commonly, posterior. The use of wide-angle viewing system combined with sclera indentation may lower the incidence of RRD by early intraoperative detection and management of peripheral retinal tears.  Vitrectomy for PDR and EFVP dissection carries a higher risk of developing retinal breaks. , The incidence of retinal breaks was 29% of eyes undergoing 20-gauge vitrectomy for PDR with tears during EFVP dissection carrying a poor outcome than peripheral retinal tears or oral dialysis.  Entry site tears are not common in small gauge vitrectomy.  Presence of Asteroid Hyalosis increase possibility of tear creation during posterior hyaloid separation and should be performed carefully in diabetic eyes. 
Postoperative RRD occurred in 12% of eyes in an earlier study;  however, in more recent studies, RD was reported in only 3-4%. ,,
| Elevated Intraocular Pressure|| |
Patients treated for TRD complicating PDR were at high-risk for prolonged postoperative IOP elevation which occurred as early as 4 h postsurgery.  This was significantly correlated with laser photocoagulation, especially in conjunction with silicon oil tamponade and combined cataract surgery. ,
| Neovascular Glaucoma|| |
Neovascular glaucoma was reported in about 3-5% of eyes post diabetic vitrectomy. , Persistent VEGF production from the severely ischemic or inadequately laser treated retina is the main drive for vasoproliferative complications of diabetic retinopathy,  Preoperative angle or iris neovascularization, postvitrectomy RD and NVG in the other eye were significant risk factors.  Repair of RD if present and/or urgent panretinal photocoagulation is the main treatment, adjuvant intravitral anti-VEGF offers a rapid, though short-term, regression of iris neovessels. , Glaucoma shunt surgery or cyclodestructive procedures may be an alternative measure for treatment of poorly controlled cases. ,
| Anterior Hyaloidal Fibrovascular Proliferation|| |
Anterior hyaloidal fibrovascular proliferation is a rare early postoperative complication of diabetic vitrectomy that needs prompt surgical treatment. Fibrovascular proliferations originating from the anterior retina and extending along the anterior hyaloid, posterior lens capsule, and may cover the pars plana, ciliary body and iris, resulting hemorrhage into the vitreous cavity, cataract, peripheral TRD, and ciliary body detachments that frequently result in atrophia bulbi with severe visual loss. , In a small case series of eyes with AHFVP, VEGF were more than 5 times higher than the baseline at the primary surgery suggesting its role in the development of AHFVP.  Young males with type I diabetes having extensive retinal ischemia and severe EFVP are predisposed to this condition. Preventive measures for patients at high-risk for this condition include peripheral retinal ablation by confluent laser treatment or cryotherapy. Surgical management for AHFVP include lensectomy, extensive dissection of anterior proliferations and the use of silicon oil tamponade. ,
| Fibrinoid Syndrome|| |
Fibrinoid syndrome is a rare postvitrectomy complication characterized by profuse outpouring of fibrin into the anterior and posterior segments of some eyes,  this may lead to several complications, including pupillary block glaucoma, elevation of intraocular pressure, and TRD.  Poor preoperative visual acuity in the absence of VH predicts, and reflects abnormalities in both preexisting visual function and integrity of the blood-ocular barrier.  When severe, intravitreal tPA,  or streptokinase  may dissolve the clot, while in more severe cases with threatening RD, repeat vitrectomy is considered [Figure 8].
|Figure 8: Fibrinoid reaction following diabetic vitrectomy, (a) first postoperative day with interconnecting fibrin strands in the vitreous cavity (nasal retinal view), (b) 20 min after intravitreal injection of tissue plasminogen activator|
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In addition to the previously described main complications of diabetic vitrectomy, some of the complications of 20-gauge vitrectomy have decreased markedly, such as corneal edema and retinal incarceration after the use of noncontact viewing system and small gauge vitrectomy. However, other complications have increased, including hypotony, serous choroidal detachment, subconjunctival silicon oil, and endophthalmitis. ,,
| Outcomes of Diabetic Vitrectomy|| |
Apart from the improvements in instrumentation and techniques of vitrectomy, the improved control and management of diabetic patients,  and the lowered threshold for surgical intervention could be contributing for the improved outcomes of diabetic vitrectomy now-a-days compared to the era of DRVS study. ,
In an interesting historical comparison of surgical outcome after diabetic vitrectomy between two studies, Newman noted that, during the 25 years separating the two studies, the proportion of good visual outcomes has increased, while the proportion of poor visual outcomes has reduced.  Visual acuity of 20/100 or better has increased from 36% to 59%, visual acuity worse than 5/200 has decreased from 30% to 16%, and no light perception has decreased from 14% to 2%. It is noteworthy to inform the patient that visual recovery is slow after diabetic vitrectomy, with a tendency for the visual acuity to change during the initial 6 months after surgery and to stabilize by 1 year.  While this delay in visual recovery could be due to the underlying retinal pathology, yet, this could also be due to surgically induced astigmatism and can be overcome by using sutureless small gauge vitrectomy. 
The results of vitrectomy for nonclearing VH have shown visual improvement in 59-83% of patients, with a final visual acuity of 20/200 or better in 40-62%.  Early vitrectomy (within 4 weeks) for subhyaloid hemorrhage appears to be associated with good visual acuity outcomes. 
Severe fibrovascular proliferations
Visual improvement is reported in 72% of cases, with about 44% achieving visual acuity of 20/40 or better. 
Traction retinal detachment
Visual improvement was reported in 59-80% of cases having macula-involving traction RD, with visual acuity of 20/200 or better achieved in 21-58.  When traction RD involves the macula, functional outcomes improved less than anatomical outcomes. Yorston et al. have reported visual improvement after vitrectomy for diabetic traction RD, with visual acuity better than 20/100 achieved in 58% of cases having macula-involving traction RD, and in 79% when the macula was not involved. 
Combined traction and rhegmatogenous retinal detachment
Visual improvement was reported in 32-53% with a final visual acuity of 20/200 or better achieved in 25-36% of cases. 
Diabetic macular edema
Diabetic retinopathy clinical research network evaluated vitrectomy for 87 eyes having diabetic macular edema associated with vitreomacular traction.  While results have shown a consistent reduction in macular thickness, visual outcome were less consistent with some eyes improving (28-49%) and some eyes worsening (13-31%).
| Prognostic Risk Factors|| |
Diabetic vitrectomy is dealing with the secondary complications of a microvascular disease. Frequently, despite a technically well-performed and anatomically successful surgery, visual outcomes remain unpredictable. Macular ischemia is difficult to assess when the posterior pole is obscured. Yorston et al. suggested that, as it is difficult to predict the visual outcome of vitrectomy for diabetic retinopathy, surgery may still be offered to patients who have a poor prognosis, as some of them will do well. 
In addition to postoperative complications, severe ischemia affecting the macula and the optic nerve or resulting in NVG and persistent and severe macular edema are the main causes of visual loss associating an anatomically successful surgery.  In one report, poor visual outcome with visual acuity of light perception or no light perception was reported in 7% of the cases.  Predictive factors of a poor visual outcome include iris neovascularization, poor preoperative visual acuity (which may be surrogate indicators of retinal ischemia and increased levels of intraocular VEGF).  Other prognostic risk factors include; macular detachment, complex fibrovascular membrane dissection (surrogate indicators comprising iatrogenic retinal breaks and use of long-acting intraocular tamponade). 
Configuration of traction RD has been found to correlate with final visual outcome. While Hammock RD and the diffuse preretinal membranes were associated with favorable outcomes, long-standing highly elevated detachments (table-top and tent form) demonstrated poorer visual outcomes. 
| Conclusion|| |
Proper medical control of blood glucose level and blood pressure as well as timely application of laser treatment for the treatment of complications of diabetic retinopathy can usually preserve vision in diabetic patients. However, in cases recalcitrant to such treatment, early vitrectomy and the use of evolving pharmacotherapy may preserve useful vision; the continuous refinement in vitrectomy instrumentation and techniques with the resultant improvement of visual outcome make pars plana vitrectomy a valuable tool for the management of late complications of PDR.
| References|| |
Klein R, Klein BE, Moss SE, Cruickshanks KJ. The Wisconsin Epidemiologic Study of Diabetic Retinopathy: XVII. The 14-year incidence and progression of diabetic retinopathy and associated risk factors in type 1 diabetes. Ophthalmology 1998;105:1801-15.
Lamri L, Gripiotis E, Ferrario A. Diabetes in Algeria and challenges for health policy: A literature review of prevalence, cost, management and outcomes of diabetes and its complications. Global Health 2014;10:11.
Zheng Y, He M, Congdon N. The worldwide epidemic of diabetic retinopathy. Indian J Ophthalmol 2012;60:428-31.
Cunha-Vaz JG, Fonseca JR, Abreu JF, Ruas MA. Detection of early retinal changes in diabetes by vitreous fluorophotometry. Diabetes 1979;28:16-9.
Sebag J. Vitreous pathobiology. In: Tasman W, Jaeger EA, editors. Duane′s Clinical Ophthalmology. Vol. 3, Ch. 39. Philadelphia: Lippincott Williams and Wilkins; 2004.
Kohno T, Sorgente N, Goodnight R, Ryan SJ. Alterations in the distribution of fibronectin and laminin in the diabetic human eye. Invest Ophthalmol Vis Sci 1987;28:515-21.
Olk RJ, Lee CM. Classification of diabetic retinopathy. In: Olk RJ, Lee CM, editors. Diabetic Retinopathy: Practical Management. Philadelphia, PA: Lippincott; 1993. p. 14-8.
Jalkh A, Takahashi M, Topilow HW, Trempe CL, McMeel JW. Prognostic value of vitreous findings in diabetic retinopathy. Arch Ophthalmol 1982;100:432-4.
Kroll P, Rodrigues EB, Hoerle S. Pathogenesis and classification of proliferative diabetic vitreoretinopathy. Ophthalmologica 2007;221:78-94.
Casaroli Marano RP, Vilaró S. The role of fibronectin, laminin, vitronectin and their receptors on cellular adhesion in proliferative vitreoretinopathy. Invest Ophthalmol Vis Sci 1994;35:2791-803.
Faulborn J, Bowald S. Microproliferations in proliferative diabetic retinopathy and their relationship to the vitreous: Corresponding light and electron microscopic studies. Graefes Arch Clin Exp Ophthalmol 1985;223:130-8.
Davis MD. Vitreous contraction in proliferative diabetic retinopathy. Arch Ophthalmol 1965;74:741-51.
Eliott D, Lee MS, Abrams GW. Proliferative diabetic retinopathy: Principles and techniques of surgical treatment. In: Ryan SJ, Hinton DR, Schachat AP, Wilkinson CP, editors. Retina. 4 th
ed. Philadelphia: Elsevier Mosby; 2006. p. 2413-49.
Ghoraba H. Types of macular holes encountered during diabetic vitrectomy. Retina 2002;22:176-82.
Ostri C, la Cour M, Lund-Andersen H. Diabetic vitrectomy in a large type 1 diabetes patient population: Long-term incidence and risk factors. Acta Ophthalmol 2013 Aug 3. Doi: 10.1111/aos.12249 (epub ahead of print).
Gupta B, Sivaprasad S, Wong R, Laidlaw A, Jackson TL, McHugh D, et al
. Visual and anatomical outcomes following vitrectomy for complications of diabetic retinopathy: The DRIVE UK study. Eye (Lond) 2012;26:510-6.
Aaberg TM, Abrams GW. Changing indications and techniques for vitrectomy in management of complications of diabetic retinopathy. Ophthalmology 1987;94:775-9.
Morse LS, Chapman CB, Eliott D, Benner JD, Blumenkranz MS, McCuen BW 2 nd
. Subretinal hemorrhage in diabetic retinopathy. Retina 1997;17:87-93.
Ziemianski MC, McMeel JW, Franks EP. Natural history of vitreous hemorrhage in diabetic retinopathy. Ophthalmology 1980;87:306-12.
Two-year course of visual acuity in severe proliferative diabetic retinopathy with conventional management. Diabetic Retinopathy Vitrectomy Study (DRVS) report #1. Ophthalmology 1985;92:492-502.
Cordido M, Fernández-Vigo J, Fandiño J, Sánchez-Salorio M. Natural evolution of massive vitreous hemorrhage in diabetic retinopathy. Retina 1988;8:96-101.
Spraul CW, Grossniklaus HE. Vitreous hemorrhage. Surv Ophthalmol 1997;42:3-39.
Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy. Two-year results of a randomized trial. Diabetic Retinopathy Vitrectomy Study report 2. The Diabetic Retinopathy Vitrectomy Study Research Group. Arch Ophthalmol 1985;103:1644-52.
Scanlon PH. Why do patients still require surgery for the late complications of proliferative diabetic retinopathy? Eye (Lond) 2010;24:435-40.
Newman DK. Surgical management of the late complications of proliferative diabetic retinopathy. Eye (Lond) 2010;24:441-9.
Charles S. Vitreous Microsurgery. 4 th
ed. Philadelphia: Williams and Wilkins; 2007. p. 95-111.
O′Hanley GP, Canny CL. Diabetic dense premacular hemorrhage. A possible indication for prompt vitrectomy. Ophthalmology 1985;92:507-11.
Ramsay RC, Knobloch WH, Cantrill HL. Timing of vitrectomy for active proliferative diabetic retinopathy. Ophthalmology 1986;93:283-9.
Kellner U, Foerster MH. Falsely nonrecordable flash visual evoked cortical potentials in a diabetic eye with severe vitreous hemorrhage. Ger J Ophthalmol 1996;5:23-5.
Kaynak S, Eryildirim A, Kaynak T, Durak I, Saatçi O, Eryildirim S, et al
. Nd: YAG laser posterior hyaloidotomy in subhyaloid hemorrhage. Ophthalmic Surg 1994;25:474-6.
Raymond LA. Neodymium: YAG laser treatment for hemorrhages under the internal limiting membrane and posterior hyaloid face in the macula. Ophthalmology 1995;102:406-11.
Celebi S, Kükner AS. Photodisruptive Nd: YAG laser in the management of premacular subhyaloid hemorrhage. Eur J Ophthalmol 2001;11:281-6.
Rennie CA, Newman DK, Snead MP, Flanagan DW. Nd: YAG laser treatment for premacular subhyaloid haemorrhage. Eye (Lond) 2001;15:519-24.
Spaide RF, Fisher YL. Intravitreal bevacizumab (Avastin) treatment of proliferative diabetic retinopathy complicated by vitreous hemorrhage. Retina 2006;26:275-8.
El-Batarny AM. Intravitreal bevacizumab treatment for retinal neovascularization and vitreous hemorrhage in proliferative diabetic retinopathy. Clin Ophthalmol 2007;1:149-55.
Arevalo JF, Maia M, Flynn HW Jr, Saravia M, Avery RL, Wu L, et al
. Tractional retinal detachment following intravitreal bevacizumab (Avastin) in patients with severe proliferative diabetic retinopathy. Br J Ophthalmol 2008;92:213-6.
Hutton WL, Bernstein I, Fuller D. Diabetic traction retinal detachment. Factors influencing final visual acuity. Ophthalmology 1980;87:1071-7.
Cohen HB, McMeel JW, Franks EP. Diabetic traction detachment. Arch Ophthalmol 1979;97:1268-72.
Charles S, Flinn CE. The natural history of diabetic extramacular traction retinal detachment. Arch Ophthalmol 1981;99:66-8.
Miller SA, Butler JB, Myers FL, Bresnick GH. Pars plana vitrectomy. Treatment for tractional macula detachment secondary to proliferative diabetic retinopathy. Arch Ophthalmol 1980;98:659-64.
Aaberg TM. Pars plana vitrectomy for diabetic traction retinal detachment. Ophthalmology 1981;88:639-42.
Smiddy WE, Flynn HW Jr. Vitrectomy in the management of diabetic retinopathy. Surv Ophthalmol 1999;43:491-507.
Diabetic Retinopathy Vitrectomy Study. Early vitrectomy for severe progressive diabetic retinopathy in eyes with useful vision. Clinical application of results of a randomized trial. Diabetic retinopathy vitrectomy study report 4. The Diabetic Retinopathy Vitrectomy Study Research Group. Ophthalmology 1988;95:1321-34.
Grewing R, Mester U. Early vitrectomy for progressive diabetic proliferations covering the macula. Br J Ophthalmol 1994;78:433-6.
Nasrallah FP, Jalkh AE, Van Coppenolle F, Kado M, Trempe CL, McMeel JW, et al
. The role of the vitreous in diabetic macular edema. Ophthalmology 1988;95:1335-9.
Hikichi T, Fujio N, Akiba J, Azuma Y, Takahashi M, Yoshida A. Association between the short-term natural history of diabetic macular edema and the vitreomacular relationship in type II diabetes mellitus. Ophthalmology 1997;104:473-8.
Lewis H, Abrams GW, Blumenkranz MS, Campo RV. Vitrectomy for diabetic macular traction and edema associated with posterior hyaloidal traction. Ophthalmology 1992;99:753-9.
Kaiser PK, Riemann CD, Sears JE, Lewis H. Macular traction detachment and diabetic macular edema associated with posterior hyaloidal traction. Am J Ophthalmol 2001;131:44-9.
Harbour JW, Smiddy WE, Flynn HW Jr, Rubsamen PE. Vitrectomy for diabetic macular edema associated with a thickened and taut posterior hyaloid membrane. Am J Ophthalmol 1996;121:405-13.
Tachi N, Ogino N. Vitrectomy for diffuse macular edema in cases of diabetic retinopathy. Am J Ophthalmol 1996;122:258-60.
Recchia FM, Ruby AJ, Carvalho Recchia CA. Pars plana vitrectomy with removal of the internal limiting membrane in the treatment of persistent diabetic macular edema. Am J Ophthalmol 2005;139:447-54.
Thomas D, Bunce C, Moorman C, Laidlaw DA. A randomised controlled feasibility trial of vitrectomy versus laser for diabetic macular oedema. Br J Ophthalmol 2005;89:81-6.
Patel JI, Hykin PG, Schadt M, Luong V, Bunce C, Fitzke F, et al.
Diabetic macular oedema: Pilot randomised trial of pars plana vitrectomy vs macular argon photocoagulation. Eye (Lond) 2006;20:873-81.
Shah SP, Patel M, Thomas D, Aldington S, Laidlaw DA. Factors predicting outcome of vitrectomy for diabetic macular oedema: Results of a prospective study. Br J Ophthalmol 2006;90:33-6.
Patel JI, Hykin PG, Schadt M, Luong V, Fitzke F, Gregor ZJ. Pars plana vitrectomy with and without peeling of the inner limiting membrane for diabetic macular edema. Retina 2006;26:5-13.
Boyer DS, Faber D, Gupta S, Patel SS, Tabandeh H, Li XY, et al
. Dexamethasone intravitreal implant for treatment of diabetic macular edema in vitrectomized patients. Retina 2011;31:915-23.
Herrero-Vanrell R, Cardillo JA, Kuppermann BD. Clinical applications of the sustained-release dexamethasone implant for treatment of macular edema. Clin Ophthalmol 2011;5:139-46.
Mitchell P, Bandello F, Schmidt-Erfurth U, Lang GE, Massin P, Schlingemann RO, et al
. The RESTORE study: Ranibizumab monotherapy or combined with laser versus laser monotherapy for diabetic macular edema. Ophthalmology 2011;118:615-25.
Machemer R, Buettner H, Norton RW, Parel JM. Vitrectomy in the management of severe diabetic retinopathies. Trans Am Acad Ophthalmol Otolayngol 1971;75:813-20.
Virata SR, Kylstra JA. Postoperative complications following vitrectomy for proliferative diabetic retinopathy with sew-on and noncontact wide-angle viewing lenses. Ophthalmic Surg Lasers 2001;32:193-7.
Schrey S, Krepler K, Wedrich A. Incidence of rhegmatogenous retinal detachment after vitrectomy in eyes of diabetic patients. Retina 2006;26:149-52.
Fujii GY, De Juan E Jr, Humayun MS, Chang TS, Pieramici DJ, Barnes A, et al
. Initial experience using the transconjunctival sutureless vitrectomy system for vitreoretinal surgery. Ophthalmology 2002;109:1814-20.
Mason JO 3 rd
, Colagross CT, Vail R. Diabetic vitrectomy: Risks, prognosis, future trends. Curr Opin Ophthalmol 2006;17:281-5.
Eckardt C. Transconjunctival sutureless 23-gauge vitrectomy. Retina 2005;25:208-211.
Khanduja S, Kakkar A, Majumdar S, Vohra R, Garg S. Small gauge vitrectomy: Recent update. Oman J Ophthalmol 2013;6:3-11.
Mccabe FJ, Regillo CD, Benson WE. Vitrectomy. In: Tasman W, Jaeger EA, editors. Duane′s Clinical Ophthalmology. Vol. 3, Ch. 56. Philadelphia: Lippincott Williams and Wilkins; 2004.
Kakehashi A. Total en bloc
excision: A modified vitrectomy technique for proliferative diabetic retinopathy. Am J Ophthalmol 2002;134:763-5.
Zinn KM. Surgical management of vitreoretinal membranes in proliferative diabetic retinopathy. Bull N Y Acad Med 1982;58:382-98.
Williamson TH. Diabetic retinopathy and other vascular disorders. In: Williamson TH, editors. Vitreoretinal Surgery. Berlin: Springer; 2008. p. 141-51.
Michels RG. Vitrectomy for complications of diabetic retinopathy. Arch Ophthalmol 1978;96:237-46.
Meredith TA, Kaplan HJ, Aaberg TM. Pars plana vitrectomy techniques for relief of epiretinal traction by membrane segmentation. Am J Ophthalmol 1980;89:408-13.
Peyman GA, Schulman JA. Diabetes mellitus. In: Peyman GA, Schulman JA, editors Intravitreal Surgery. Principles and Practice. 2 nd
ed. Norwalk, Connecticut: Appleton and Lange; 1994. p. 419-87.
Charles S. Vitreous Microsurgery. Baltimore: Williams and Wilkins; 1981. p. 115.
Meredith TA. Epiretinal membrane delamination with a diamond knife. Arch Ophthalmol 1997;115:1598-9.
Kadonosono K, Yamakawa T, Uchio E, Watanabe Y, Yanagi Y, Tamaki Y, et al
. Fibrovascular membrane removal using a high-performance 25-gauge vitreous cutter. Retina 2008;28:1533-5.
Charles S. Vitreous Microsurgery. 1 st
ed. Baltimore: Williams and Wilkins; 1981. p. 107-20.
McCuen BW 2 nd
, Hickingbotham D. A fiberoptic diathermy tissue manipulator for use in vitreous surgery. Am J Ophthalmol 1984;98:803-4.
Pendergast SD, Martin DF, Proia AD, Jaffe GJ, McCuen BW 2 nd
. Removal of optic disc stalks during diabetic vitrectomy. Retina 1995;15:25-8.
Abrams GW, Williams GA. "En bloc
" excision of diabetic membranes. Am J Ophthalmol 1987;103:302-8.
Han DP, Murphy ML, Mieler WF. A modified en bloc
excision technique during vitrectomy for diabetic traction retinal detachment. Results and complications. Ophthalmology 1994;101:803-8.
Quiroz-Mercado H, Guerrero-Naranjo J, Agurto-Rivera R, Leizaola-Fernández C, Suárez-Tatá L, Murillo-López S, et al
. Perfluorocarbon-perfused vitrectomy: A new method for vitrectomy - A safety and feasibility study. Graefes Arch Clin Exp Ophthalmol 2005;243:551-62.
Arevalo JF. En bloc
perfluorodissection for tractional retinal detachment in proliferative diabetic retinopathy. Ophthalmology 2008;115:e21-5.
Shinoda K, Inoue M, Katsura H, Ishida S. A new technique for separation of posterior vitreous in vitreous surgery. Ophthalmic Surg Lasers 1999;30:588-90.
Grigorian RA, Castellarin A, Fegan R, Seery C, Del Priore LV, Von Hagen S, et al
. Epiretinal membrane removal in diabetic eyes: Comparison of viscodissection with conventional methods of membrane peeling. Br J Ophthalmol 2003;87:737-41.
Lincoff H, Coleman J, Kreissig I, Richard G, Chang S, Wilcox LM. The perfluorocarbon gases in the treatment of retinal detachment. Ophthalmology 1983;90:546-51. Cited In: Peyman GA, Schulman JA, editors. Intravitreal Surgery. Principles and practice. 2 nd
ed. Norwalk, Connecticut: Appleton and Lange; 1994. p. 70.
Kaymak H. Long term follow-up with a new endotamponade. Vitreoretinal surgery poster presentations. Proceedings of the 10 th
EURETINA Congress. Paris; September, 2010.
Caramoy A, Schröder S, Fauser S, Kirchhof B. In vitro
emulsification assessment of new silicone oils. Br J Ophthalmol 2010;94:509-12.
Caramoy A, Hagedorn N, Fauser S, Kugler W, Gross T, Kirchhof B. Development of emulsification-resistant silicone oils: Can we go beyond 2000 mPas silicone oil? Invest Ophthalmol Vis Sci 2011;52:5432-6.
Sharma YR, Pruthi A, Azad RV, Kumar A, Mannan R. Impact of early rise of intraocular pressure on visual outcome following diabetic vitrectomy. Indian J Ophthalmol 2011;59:37-40.
Zaninetti M, Petropoulos IK, Pournaras CJ. Proliferative diabetic retinopathy: Vitreo-retinal complications are often related to insufficient retinal photocoagulation. J Fr Ophtalmol 2005;28:381-4.
Yorston D, Wickham L, Benson S, Bunce C, Sheard R, Charteris D. Predictive clinical features and outcomes of vitrectomy for proliferative diabetic retinopathy. Br J Ophthalmol 2008;92:365-8.
Brourman ND, Blumenkranz MS, Cox MS, Trese MT. Silicone oil for the treatment of severe proliferative diabetic retinopathy. Ophthalmology 1989;96:759-64.
Castellarin A, Grigorian R, Bhagat N, Del Priore L, Zarbin MA. Vitrectomy with silicone oil infusion in severe diabetic retinopathy. Br J Ophthalmol 2003;87:318-21.
Sebag J. Anomalous posterior vitreous detachment: A unifying concept in vitreo-retinal disease. Graefes Arch Clin Exp Ophthalmol 2004;242:690-8.
Schwatz SD, Alexander R, Hiscott P, Gregor ZJ. Recognition of vitreoschisis in proliferative diabetic retinopathy. A useful landmark in vitrectomy for diabetic traction retinal detachment. Ophthalmology 1996;103:323-8.
Chu TG, Lopez PF, Cano MR, Freeman WR, Lean JS, Liggett PE, et al
. Posterior vitreoschisis. An echographic finding in proliferative diabetic retinopathy. Ophthalmology 1996;103:315-22.
Sonoda KH, Sakamoto T, Enaida H, Miyazaki M, Noda Y, Nakamura T, et al
. Residual vitreous cortex after surgical posterior vitreous separation visualized by intravitreous triamcinolone acetonide. Ophthalmology 2004;111:226-30.
Yeh PT, Yang CM, Yang CH. Distribution, reabsorption, and complications of preretinal blood under silicone oil after vitrectomy for severe proliferative diabetic retinopathy. Eye (Lond) 2012;26:601-8.
Imamura Y, Kamei M, Minami M, Ueki M, Ikeda T. Heparin-assisted removal of clotting preretinal hemorrhage during vitrectomy for proliferative diabetic retinopathy. Retina 2005;25:793-5.
Grusha YO, Masket S, Miller KM. Phacoemulsification and lens implantation after pars plana vitrectomy. Ophthalmology 1998;105:287-94.
Rivas-Aguiño P, García-Amaris RA, Berrocal MH, Sánchez JG, Rivas A, Arévalo JF. Pars plana vitrectomy, phacoemulsification and intraocular lens implantation for the management of cataract and proliferative diabetic retinopathy: Comparison of a combined versus two-step surgical approach. Arch Soc Esp Oftalmol 2009;84:31-8.
Blankenship GW. The lens influence on diabetic vitrectomy results. Report of a prospective randomized study. Arch Ophthalmol 1980;98:2196-8.
Lahey JM, Francis RR, Kearney JJ. Combining phacoemulsification with pars plana vitrectomy in patients with proliferative diabetic retinopathy: A series of 223 cases. Ophthalmology 2003;110:1335-9.
Treumer F, Bunse A, Rudolf M, Roider J. Pars plana vitrectomy, phacoemulsification and intraocular lens implantation. Comparison of clinical complications in a combined versus two-step surgical approach. Graefes Arch Clin Exp Ophthalmol 2006;244:808-15.
Kuppermann BD, Thomas EL, de Smet MD, Grillone LR, Vitrase for Vitreous Hemorrhage Study Groups. Pooled efficacy results from two multinational randomized controlled clinical trials of a single intravitreous injection of highly purified ovine hyaluronidase (Vitrase) for the management of vitreous hemorrhage. Am J Ophthalmol 2005;140:573-84.
Kuppermann BD, Thomas EL, de Smet MD, Grillone LR, Vitrase for Vitreous Hemorrhage Study Groups. Safety results of two phase III trials of an intravitreous injection of highly purified ovine hyaluronidase (Vitrase) for the management of vitreous hemorrhage. Am J Ophthalmol 2005;140:585-97.
Hirata A, Takano A, Inomata Y, Yonemura N, Sagara N, Tanihara H. Plasmin-assisted vitrectomy for management of proliferative membrane in proliferative diabetic retinopathy: A pilot study. Retina 2007;27:1074-8.
Murakami T, Takagi H, Ohashi H, Kita M, Nishiwaki H, Miyamoto K, et al
. Role of posterior vitreous detachment induced by intravitreal tissue plasminogen activator in macular edema with central retinal vein occlusion. Retina 2007;27:1031-7.
Benz MS, Packo KH, Gonzalez V, Pakola S, Bezner D, Haller JA, et al
. A placebo-controlled trial of microplasmin intravitreous injection to facilitate posterior vitreous detachment before vitrectomy. Ophthalmology 2010;117:791-7.
Schachat AP, Oyakawa RT, Michels RG, Rice TA. Complications of vitreous surgery for diabetic retinopathy. II. Postoperative complications. Ophthalmology 1983;90:522-30.
Lee BJ, Yu HG. Vitreous hemorrhage after the 25-gauge transconjunctival sutureless vitrectomy for proliferative diabetic retinopathy. Retina 2010;30:1671-7.
West JF, Gregor ZJ. Fibrovascular ingrowth and recurrent haemorrhage following diabetic vitrectomy. Br J Ophthalmol 2000;84:822-5.
Yan H, Cui J, Lu Y, Yu J, Chen S, Xu Y. Reasons for and management of postvitrectomy vitreous hemorrhage in proliferative diabetic retinopathy. Curr Eye Res 2010;35:308-13.
Novak MA, Rice TA, Michels RG, Auer C. Vitreous hemorrhage after vitrectomy for diabetic retinopathy. Ophthalmology 1984;91:1485-9.
Yeh PT, Yang CM, Yang CH, Huang JS. Cryotherapy of the anterior retina and sclerotomy sites in diabetic vitrectomy to prevent recurrent vitreous hemorrhage: An ultrasound biomicroscopy study. Ophthalmology 2005;112:2095-102.
Khuthaila MK, Hsu J, Chiang A, DeCroos FC, Milder EA, Setlur V, et al
. Postoperative vitreous hemorrhage after diabetic 23-gauge pars plana vitrectomy. Am J Ophthalmol 2013;155:757-63.
Park DH, Shin JP, Kim SY. Comparison of clinical outcomes between 23-gauge and 20-gauge vitrectomy in patients with proliferative diabetic retinopathy. Retina 2010;30:1662-70.
Lee DY, Jeong HS, Sohn HJ, Nam DH. Combined 23-gauge sutureless vitrectomy and clear corneal phacoemulsification in patients with proliferative diabetic retinopathy. Retina 2011;31:1753-8.
Yang CM, Yeh PT, Yang CH, Chen MS. Bevacizumab pretreatment and long-acting gas infusion on vitreous clear-up after diabetic vitrectomy. Am J Ophthalmol 2008;146:211-7.
da R Lucena D, Ribeiro JA, Costa RA, Barbosa JC, Scott IU, de Figueiredo-Pontes LL, et al
. Intraoperative bleeding during vitrectomy for diabetic tractional retinal detachment with versus without preoperative intravitreal bevacizumab (IBeTra study). Br J Ophthalmol 2009;93:688-91.
Romano MR, Gibran SK, Marticorena J, Wong D, Heimann H. Can an intraoperative bevacizumab injection prevent recurrent postvitrectomy diabetic vitreous hemorrhage? Eur J Ophthalmol 2009;19:618-21.
Carter JB, Michels RG, Glaser BM, De Bustros S. Iatrogenic retinal breaks complicating pars plana vitrectomy. Ophthalmology 1990;97:848-53.
Kamura Y, Sato Y, Deguchi Y, Yagi F. Iatrogenic retinal breaks during 20-gauge vitrectomy for proliferative diabetic retinopathy. Clin Ophthalmol 2013;7:29-33.
Ehrlich R, Goh YW, Ahmad N, Polkinghorne P. Retinal breaks in small-gauge pars plana vitrectomy. Am J Ophthalmol 2012;153:868-72.
Ikeda T, Sawa H, Koizumi K, Yasuhara T, Kinoshita S, Tano Y. Vitrectomy for proliferative diabetic retinopathy with asteroid hyalosis. Retina 1998;18:410-4.
Muether PS, Hoerster R, Kirchhof B, Fauser S. Course of intraocular pressure after vitreoretinal surgery: Is early postoperative intraocular pressure elevation predictable? Retina 2011;31:1545-52.
Hasegawa Y, Okamoto F, Sugiura Y, Okamoto Y, Hiraoka T, Oshika T. Intraocular pressure elevation after vitrectomy for various vitreoretinal disorders. Eur J Ophthalmol 2014;24:235-41.
Helbig H, Kellner U, Bornfeld N, Foerster MH. Rubeosis iridis after vitrectomy for diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol 1998;236:730-3.
Goto A, Inatani M, Inoue T, Awai-Kasaoka N, Takihara Y, Ito Y, et al
. Frequency and risk factors for neovascular glaucoma after vitrectomy in eyes with proliferative diabetic retinopathy. J Glaucoma 2013;22:572-6.
Avery RL, Pearlman J, Pieramici DJ, Rabena MD, Castellarin AA, Nasir MA, et al
. Intravitreal bevacizumab (Avastin) in the treatment of proliferative diabetic retinopathy. Ophthalmology 2006;113:1695.e1-15.
Ehlers JP, Spirn MJ, Lam A, Sivalingam A, Samuel MA, Tasman W. Combination intravitreal bevacizumab/panretinal photocoagulation versus panretinal photocoagulation alone in the treatment of neovascular glaucoma. Retina 2008;28:696-702.
Lloyd MA, Heuer DK, Baerveldt G, Minckler DS, Martone JF, Lean JS, et al
. Combined Molteno implantation and pars plana vitrectomy for neovascular glaucomas. Ophthalmology 1991;98:1401-5.
Simmons RB, Shields MB, Blasini M, Wilkerson M, Stern RA. Transscleral Nd: YAG laser cyclophotocoagulation with a contact lens. Am J Ophthalmol 1991;112:671-7.
Lewis H, Abrams GW, Williams GA. Anterior hyaloidal fibrovascular proliferation after diabetic vitrectomy. Am J Ophthalmol 1987;104:607-13.
Lewis H, Abrams GW, Foos RY. Clinicopathologic findings in anterior hyaloidal fibrovascular proliferation after diabetic vitrectomy. Am J Ophthalmol 1987;104:614-8.
Kobayashi T, Machida S, Fujiwara T, Ishibe T, Kurosaka D. Vitreous levels of vascular endothelial growth factor in eyes with anterior hyaloidal fibrovascular proliferation. Clin Ophthalmol 2010;4:1043-6.
Sebestyen JG. Fibrinoid syndrome: A severe complication of vitrectomy surgery in diabetics. Ann Ophthalmol 1982;14:853-6.
Han DP, Wang Q, Hartz A, Jaffe GJ, Murray TG, Boldt HC, et al
. Postoperative fibrin formation and visual outcome after pars plana vitrectomy. Retina 1994;14:225-30.
Williams GA, Lambrou FH, Jaffe GA, Snyder RW, Green GD, Devenyi RG, et al
. Treatment of postvitrectomy fibrin formation with intraocular tissue plasminogen activator. Arch Ophthalmol 1988;106:1055-8.
Cherfan GM, el Maghraby A, Tabbara KF, Nasr Y, Hassan H. Dissolution of intraocular fibrinous exudate by streptokinase. Ophthalmology 1991;98:870-4.
Shaikh S, Ho S, Richmond PP, Olson JC, Barnes CD. Untoward outcomes in 25-gauge versus 20-gauge vitreoretinal surgery. Retina 2007;27:1048-53.
Farouk MM, Naito T, Sayed KM, Nagasawa T, Katome T, Radwan G, et al
. Outcomes of 25-gauge vitrectomy for proliferative diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol 2011;249:369-76.
Erakgun T, Egrilmez S. Surgical outcomes of transconjunctival sutureless 23-gauge vitrectomy with silicone oil injection. Indian J Ophthalmol 2009;57:105-9.
Thompson JT, de Bustros S, Michels RG, Rice TA, Glaser BM. Results of vitrectomy for proliferative diabetic retinopathy. Ophthalmology 1986;93:1571-4.
Nakazawa M, Kimizuka Y, Watabe T, Kato K, Watanabe H, Yamanobe S, et al
. Visual outcome after vitrectomy for diabetic retinopathy. A five-year follow-up. Acta Ophthalmol (Copenh) 1993;71:219-23.
Kadonosono K, Yamakawa T, Uchio E, Yanagi Y, Tamaki Y, Araie M. Comparison of visual function after epiretinal membrane removal by 20-gauge and 25-gauge vitrectomy. Am J Ophthalmol 2006;142:513-5.
Diabetic Retinopathy Clinical Research Network Writing Committee, Haller JA, Qin H, Apte RS, Beck RR, Bressler NM, et al
. Vitrectomy outcomes in eyes with diabetic macular edema and vitreomacular traction. Ophthalmology 2010;117:1087-10933.
Mason JO 3 rd
, Colagross CT, Haleman T, Fuller JJ, White MF, Feist RM, et al
. Visual outcome and risk factors for light perception and no light perception vision after vitrectomy for diabetic retinopathy. Am J Ophthalmol 2005;140:231-5.
Wakabayashi Y, Usui Y, Okunuki Y, Ueda S, Kimura K, Muramatsu D, et al
. Intraocular VEGF level as a risk factor for postoperative complications after vitrectomy for proliferative diabetic retinopathy. Invest Ophthalmol Vis Sci 2012;53:6403-10.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]