Vitreoretinal Adhesion Research Articles

Extrafoveal traction in retinal vein occlusion using spectral domain optical coherence tomography

To present extrafoveal vitreous traction membranes, and their prevalence and association with diffuse macular oedema in eyes with retinal vein occlusion (RVO), using 3-D spectral-domain optical coherence tomography (SD-OCT). In a retrospective institutional observational study, charts and qualified SD-OCT findings of consecutive patients with either central retinal vein occlusion (CRVO) or branch retinal vein occlusion (BRVO) associated with macular oedema were analyzed. Exclusion criteria covered eyes that had: 1) another retinopathy that could affect the data analysis, 2) vitreoretinal adherence without signs of retinal traction, 3) undergone vitreoretinal surgery, or 4) been treated by intravitreal administration of medication(s). An age-matched control group (n = 72) afforded the normal central subfield thickness. Twenty-six eyes (of 26 patients) with either CRVO (n = 12) or BRVO (n = 14) were analyzed. Four eyes were excluded because they had a lack of macular oedema (n = 2), had an earlier pars plana vitrectomy (n = 1), or had previous treatment by intravitreal bevacizumab (n = 1). Of the 22 remaining eyes, both the SD-OCT B-mode video clip and the 3-D image reconstruction enabled a detection of extrafoveal traction membranes, either unifocally or multifocally, in nine eyes: four (of 11; 36.4 %) in CRVO, and five eyes (of 11; 45.5%) in BRVO. The retinal oedema in these nine eyes, which underlined at least one of the traction sites per eye, and the accompanied subretinal fluid in four of these nine eyes, were in continuum in each eye with the diffuse macular oedema and serous macular detachment respectively. During follow-up, a spontaneous release of a traction membrane coupled with resolution of the macular oedema occurred in one eye with BRVO. Of the four eyes that were excluded, two eyes had extrafoveal vitreous traction membranes. The SD-OCT B-mode video clip and its 3-D image reconstruction enabled relatively frequent detection of extrafoveal vitreous traction membranes in RVO and their association with diffuse macula oedema and macular detachment. A larger cohort is required to validate these findings and to compare the efficacy of early release of such traction membranes, either surgically or possibly by pharmacologic vitreolysis, with the current therapeutic modalities.

Dispase‐assisted vitrectomy for epiretinal prostheses implantation

Editor, We previously reported about a new surgical method for the implantation of epiretinal prostheses in porcine eyes (Ivastinovic et al. 2010a). While performing vitrectomy as part of the implantation procedure, we noted a strong vitreoretinal adherence hampering a complete removal of the posterior vitreous cortex. However, close proximity between the electrodes and ganglion cells is crucial for successful induction of visual perception with epiretinal implants (de Balthasar et al. 2008). Although in elderly humans posterior vitreous detachment (PVD) is commonly observed during vitrectomy, vitreoschisis might occur at different levels owing to the multilamellar structure of the posterior hyaloid (Sebag 2008). Hence, considerable amounts of vitreous remnants might still remain attached to the inner limiting lamina (ILL). Intravitreal pharmacological adjuncts, such as plasmin and dispase, have been shown to facilitate PVD. While plasmin hydrolyses laminin and fibronectin, which play key roles in the vitreoretinal attachment, dispase additionally degrades type IV collagen in the ILL, which supports the attachment of the vitreous cortex to the ILL (Wang et al. 2004). The incidence of dispase-related complications including preretinal haemorrhage, vitreous inflammation and morphological retinal damage proved to be dose dependent and more likely to occur after prolonged exposure (Wang et al. 2004). To obviate these adverse effects, the injected dose of dispase should not exceed 50 μg, and the incubation should be limited at 15 min (Oliviera et al. 2001). The aim of our study was to evaluate the efficacy and safety of 50 μg dispase at the proposed exposure in porcine eyes with respect to epiretinal prostheses implantation. We performed an experimental study in eight domestic pigs weighting 20–25 kg. This animal trial was approved by the Austrian legal authorities and the Medical University of Graz. The animals were treated according to guidelines of the Association for Research in Vision and Ophthalmology. Surgeries were performed under sterile conditions in general anaesthesia using standard parameters. One day before surgery, dispase (isolated from Bacillus polymyxa; Roche Diagnostics, Grenzach-Wyhlen, Germany) was diluted with phosphate-buffered saline to 50 μg/0.05 ml (pH = 7.4) under sterile conditions and stored at +4°C. After core vitrectomy, dispase was injected into the midvitreous cavity. The sclerotomies were temporarily closed, and the infusion stopped. After incubation of 15 min, the remaining vitreous was carefully removed. Clinical examination with indirect ophthalmoscopy was performed in general anaesthesia 4–6 weeks after surgery. After painless euthanization, the eyes were enucleated and processed for histological and immunohistochemical examination for glial fibrillary acidic protein (GFAP) to explore the extent of retinal damage. After dispase injection, PVD was induced with suction of the cutter, and the remaining vitreous could easily be removed in all animals. In four eyes, we observed spontaneous preretinal haemorrhage (Fig. 1). After the observation period, no obvious retinal pathology, such as disruption of ILL, was noted clinically. The vitreous cavity was clear in five eyes; three eyes showed a visible vitreous haze. On histological examination, complete vitreoretinal dehiscence was observed in six eyes while two eyes showed slight strands of the posterior hyaloid (Fig. 2). The vitreous haze consisted of a fibrin meshwork with inflammatory cells (Fig. 3). Immunohistochemistry revealed slight GFAP upregulation in the inner retina (Fig. 2C). Spontaneous preretinal capillary haemorrhage after dispase injection. The haemorrhage ceased intraoperatively after increasing the intraocular pressure by raising the infusion bottle. (A) Extreme periphery of the retina and pars plana. Note complete removal of posterior hyaloid. (B) Slight remnants of the posterior vitreous cortex partially attached to inner limiting lamina (arrowhead). (C) Upregulation of glial fibrillary acidic protein (GFAP) in the inner retina (arrowhead). [The samples were stained with Elastica van Gieson and haematoxylin-eosin. Immunohistochemistry was performed with GFAP antibodies. The choroidal and retinal detachment (A) is a processing artefact. Bars measure 100 μm]. Incomplete removal of posterior hyaloid and fibrin meshwork. The rectangle displays a macrophage in higher magnification. The retinal and vascular morphology is intact. [Elastica van Gieson stain. Bar measures 100 μm]. We used dispase in our study because of its commercial availability at relatively low costs. Intravitreal injection of 50 μg dispase (0.025 U) with an exposure of 15 min facilitates the complete removal of the posterior vitreous cortex and would provide a close contact between the epiretinal implant and the inner retina. However, hydrolysis of the extravascular matrix causing preretinal haemorrhage and immune response to dispase as a foreign protein still remain a concern. The extent of GFAP upregulation in our study corresponds to GFAP upregulation after vitrectomy alone (Ivastinovic et al. 2010b). In conclusion, though no structural retinal damage was observed, we do not recommend dispase as pharmacological adjunct in humans undergoing epiretinal prostheses implantation due its potential toxicity.

Spectral domain optical coherence tomography for higher precision in the evaluation of vitreoretinal adhesions in exudative age-related macular degeneration

AimThe role of changes at the vitreoretinal interface and vitreomacular traction forces in pathogenesis, and the course of exudative age-related macular degeneration (AMD) need further exploration. This study examines the...

Diagnosing and Treating Vitreomacular Adhesion

Perifoveal vitreous detachment with residual vitreofoveal adhesion is considered as the first stage of posterior vitreous detachment. A key point is the transition from an innocuous vitreomacular adhesion (VMA) to a pathological vitreomacular traction (VMT). By using optical coherence tomography (OCT), VMA is defined as adhesion of the posterior hyaloid cortex involving the centre of the foveal region with or without a hyper-reflective signal on the inner surface of the retina. VMT is diagnosed when the inner macular surface slopes steeply, or sharp angulation and localised deformation of the retinal profile is detected at the VMA site. Otherwise, VMA is simply considered to be persistent adherence of the cortical vitreous. The tractional effects of perifoveal vitreous detachment cause a variety of macular pathologies determined by the size and the strength of the residual vitreoretinal adhesion. Vitreomacular adhesion plays a major role in the development of diseases such as vitreomacular traction syndrome (VMTS), macular hole, epiretinal membrane, tractional macular oedema and myopic macular retinoschisis. In addition, clinical evidence supports the theory that the course of diabetic retinopathy and age-related macular degeneration may be strongly influenced by an incomplete posterior vitreous separation. The current standard of care of vitreomacular interface pathologies is vitrectomy and membrane peeling – a procedure that is thought to relieve epiretinal traction – followed by regeneration of the retinal architecture and recovery of visual function. Over the last few years, with the introduction of 25-gauge (0.50mm) and 23-gauge (0.72mm) instruments, there has been another major shift toward transconjunctival microincisional vitrectomy surgery (MIVS). Pharmacological induction of posterior vitreous detachment (PVD) can become a further step toward a real ‘minimally invasive vitreous surgery’ for VMTS.

Centrifugal enlargement of macular hole and macular detachment in a patient with bilateral giant macular holes.

To report the detailed vitreomacular morphology of a case of progressive enlargement and macular detachment secondary to and several years after the development of bilateral giant macular holes using optical coherence tomography. Using optical coherence tomography, both eyes of a patient with bilateral giant macular holes were examined. A 33-year-old woman had bilateral giant macular holes at the first visit. At the 5-year follow-up visit, the macular hole had enlarged centrifugally in the right eye, and a macular detachment developed beyond the arcade vessels in the left eye. Optical coherence tomography showed retinoschisis in the right eye around the edges of the hole and a macular detachment in the left eye with vitreoretinal adhesion temporal to both holes. These optical coherence tomography findings suggested that vitreomacular traction at the temporal edge of the hole may have resulted in progressive centrifugal enlargement of the hole in both eyes and then the macular detachment occurred in the left eye.

PATHOGENESIS OF RHEGMATOGENOUS RETINAL DETACHMENT

The pathogenesis of rhegmatogenous retinal detachment is complex, and our knowledge of the exact mechanism of vitreoretinal attachment and detachment remains incomplete. We performed a Medline, Ovid, and EMBASE search using search words rhegmatogenous, retinal detachment, vitreous, and retinal adhesion. All appropriate articles were reviewed, and the evidence was compiled. Cortical vitreous contains fibrillar collagens type II, V/XI, and IX. The inner limiting membrane of the retina contains collagens type I, IV, VI, and XVIII as well as numerous other glycoproteins and potential adhesion molecules. The distribution and age-related changes in the structure of these molecules play an important role in the formation of a retinal break, which may compromise and disrupt the normal mechanisms of neurosensory retinal adhesion. Rhegmatogenous retinal detachment development is intimately related to changes in the fibrillar structure of the aging vitreous culminating in posterior vitreous detachment with regions of persistent and tangential vitreoretinal traction predisposing to retinal tear formation. A complex interplay of factors such as weakening of vitreoretinal adhesion, posterior migration of the vitreous base, and molecular changes at the vitreoretinal interface are important in predisposing to focal areas of vitreoretinal traction precipitating rhegmatogenous retinal detachment. Once formed, the passage of liquefied vitreous through a retinal break may overwhelm normal neurosensory-retinal pigment epithelium adhesion perpetuating and extending detachment and causing visual loss. To understand the molecular events underlying rhegmatogenous retinal detachment so that new therapies can be developed, it is important to appreciate the structural organization of the vitreous, the biology underlying vitreous liquefaction and posterior vitreous detachment, and the mechanisms of vitreoretinal attachment and detachment.

Metabolic physiology in age related macular degeneration

Ischemia and hypoxia have been implicated in the pathophysiology of age related macular degeneration (AMD). This has mostly been based on studies on choroidal perfusion, which is not the only contributor to retinal hypoxia found in AMD eyes. Other features of AMD may also interfere with retinal oxygen metabolism including confluent drusen, serous or hemorrhagic retinal detachment, retinal edema and vitreoretinal adhesion. Each of these features contributes to retinal hypoxia: the drusen and retinal elevation by increasing the distance between the choriocapillaris and retina; vitreoretinal adhesion by reducing diffusion and convection of oxygen towards and vascular endothelial growth factor (VEGF) away from hypoxic retinal areas. Hypoxia-inducible-factor is known to exist in subretinal neovascularization and hypoxia is the main stimulus for the production of VEGF. Each feature may not by itself create enough hypoxia and VEGF accumulation to stimulate wet AMD, but they may combine to do so. Choroidal ischemia in AMD has been demonstrated by many researchers, using different technologies. Choroidal ischemia obviously decreases oxygen delivery to the outer retina. Confluent drusen, thickening of Bruch's membrane and any detachment of retina or retinal pigment epithelium, increases the distance between the choriocapillaris and the retina and thereby reduces the oxygen flux from the choroid to the outer retina according to Fick's law of diffusion. Retinal elevation and choroidal ischemia may combine forces to reduce choroidal oxygen delivery to the outer retina, produce retinal hypoxia. Hypoxia leads to production of VEGF leading to neovascularization and tissue edema. A vicious cycle may develop, where VEGF production increases effusion, retinal detachment and edema, further increasing hypoxia and VEGF production. Adhesion of the viscous posterior vitreous cortex to the retina maintains a barrier to diffusion andconvection currents in the vitreous cavity according to the laws of Fick's, Stokes-Einstein and Hagen-Poiseuille. If the vitreous is detached from the surface of the retina, the low viscosity fluid transports oxygen and nutrients towards an ischemic area of the retina, and cytokines away from the retina, at a faster rate than through attached vitreous gel. Vitreoretinal adhesion can exacerbate retinal hypoxia and accumulation of cytokines, such as VEGF. Vitreoretinal traction can also cause hypoxia by retinal elevation. Conceivably, the basic features of AMD, drusen, choroidal ischemia, and vitreoretinal adhesion are independently determined by genetics and environment and may combine in variable proportions. If the resulting hypoxia and consequent VEGF accumulation crosses a threshold, this will trigger effusion and neovascularization.

Der Einfluss des Glaskörpers auf die Pathogenese der altersabhängigen Makuladegeneration

Age-related macular degeneration (AMD) is the main cause of severe visual decease in elderly people in the industrialised countries. AMD is a multifactorial disease with only limited therapeutic options before anti-VEGF treatment was introduced. In spite of all the progress no long-term healing is possible. Actually, the vitreous is being investigated as a possible co-factor in the pathogenesis of AMD. Numerous authors demonstrated a higher incidence of vitreoretinal adhesion in exudative AMD by considering age, genetic and environmental factors. The essential question is whether the therapeutic release of vitreoretinal adhesion could affect the development and progress of AMD. Up to now only case reports and case series have demonstrated a positive effect on disease progress. An ongoing multicentre, prospective, comparative, randomised, double-blind clinical trial with enzymatic vitreolysis is now evaluting the effect of vitreoretinal release on the progress of AMD. The results are necessary to evaluate whether vitreoretinal release is a therapeutic option for the future.

Giant Macular Hole in Alport Syndrome

Purpose: To describe the evolution of a giant macular hole in a patient with Alport syndrome and review the literature.Methods: An observational case report is presented with serial clinical examination, visual acuity, fundus photographs, and ocular coherence tomography performed.Results: A man with Alport syndrome and a giant macular hole in one eye developed multiple, small lamellar macular holes which coalesced into a giant full thickness macular hole in the contralateral eye.Conclusions: Giant macular holes may occur in Alport syndrome. The mechanism and clinical progression appear to differ from that of idiopathic macular holes and, is likely related to an abnormality in Type IV collagen in basement membrane of retinal Muller cells. Anomalous vitreoretinal adhesion may also play a role. Previous cases of giant macular holes in the literature may not have been properly associated with Alport syndrome.

Ocular Hemorrhages in Neonatal Porcine Eyes from Single, Rapid Rotational Events

To characterize ocular hemorrhages from single, rapid head rotations in the neonatal pig. Three- to 5-day-old anesthetized piglets (n=51) underwent a single, rapid (117-266 rad/s) head rotation in the sagittal (n=13), coronal (n=7), or axial (n=31) planes. Six hours after injury, the animals were euthanatized and perfusion fixed, and the brain and eyes were harvested for gross and histopathologic examination by masked neuro- and ocular pathologists. Ocular hemorrhage was found in 73% of animals (51% bilateral). Intraocular hemorrhage was primarily located near the vitreous base (70% of injured animals had ciliary body hemorrhage, and 11% had peripheral retinal hemorrhage). Hemorrhages were also found in the anterior chamber (11%), vitreous (5%), and optic nerve (disc, 8%; nerve sheath, 57%). Rapid axial head rotations resulted in a higher incidence of intraocular hemorrhage than coronal or sagittal head rotations, but the difference did not reach statistical significance (P=0.06). Control eyes had no injuries. Optic nerve sheath and ciliary body hemorrhages were common in piglets that experienced a single, rapid head rotation. Retinal hemorrhage was present in a smaller number of animals. Most intraocular hemorrhages were located in regions of strong vitreous attachment, suggesting that this animal model will be useful in investigating the effect of vitreoretinal adhesion on ocular hemorrhage caused by inertial head rotations. Extrapolation of this model to the human infant should not be made until the effect of anatomic differences between the human and pig on the occurrence and patterns of ocular injuries is further investigated.

Macular appearance after diabetic vitrectomy for fibrovascular proliferation: an optical coherence tomography study

To investigate morphological variations in the macular area with optical coherence tomography (OCT) after vitrectomy for diabetic fibrovascular proliferation. We reviewed 108 cases using OCT 7-15 months after vitrectomy. Of these, 32 received OCT within 3 months postoperatively. Morphological variations were categorized and correlated with visual outcome. Only 24 cases (21.4%) had no obvious abnormalities. The most frequent findings were epiretinal membrane (52.8%), macular thickening (37.0%) and macular cysts (28.7%). Multivariate regression showed that diffuse macular thickening, loss of foveal depression and diffuse retinal thinning were significantly associated with poor visual acuity. Sequential OCT (< 3 and >or= 7 months) revealed that epiretinal membrane and oedema outside of fovea changed significantly between two examinations. OCT may identify diverse morphological changes in the macular area after diabetic vitrectomy for fibrovascular proliferation. Macular appearance may change over time, and certain types of morphological changes may be associated with poor visual function.

Posterior Vitreous Detachment: Evolution and Complications of Its Early Stages

To summarize emerging concepts regarding the onset and progression, traction effects, and complications of the early stages of age-related posterior vitreous detachment (PVD). Interpretive essay. Review and synthesis of selected literature, with clinical illustrations, interpretation, and perspective. Imaging of the vitreoretinal interface with optical coherence tomography has shown that PVD begins in the perifoveal macula. Recent longitudinal studies have demonstrated conclusively that early PVD stages persist chronically and progress slowly over months to years. Vitreous traction forces resulting from perifoveal PVD with a small vitreofoveolar adhesion (500 microm or less) may cause localized cystoid foveal thickening or one of several macular hole conditions. Traction associated with larger adhesion zones may cause or exacerbate a separate group of macular disorders. Ultrastructural studies suggest that epiretinal membrane develops from cortical vitreous remnants left on the retinal surface after PVD and plays an important role in traction vitreomaculopathies. Age-related PVD is an insidious, chronic event that begins in the perifoveal macula and evolves over a prolonged period before vitreopapillary separation. Although asymptomatic in most individuals, its early stages may be complicated by a variety of macular and optic disc pathologic features, determined in part by the size and strength of the residual vitreoretinal adhesion.

Axial length and intraoperative posterior vitreous detachment as predictive factors for surgical outcomes of diabetic vitrectomy

To evaluate the relationship of axial length (AXL), intraoperatively assessed posterior vitreous detachment (PVD) status, and surgical outcomes of diabetic vitrectomy. Retrospective, consecutive case series. Clinical records were reviewed for 115 eyes (50 males, 65 females) with more than a 6-month follow-up who underwent diabetic vitrectomy from a single surgeon. Thirty-three eyes had vitreous haemorrhage, 37 had tractional retinal detachment (TRD) threatening the macula, 43 had TRD involving the macula, and two had neovascular glaucoma. AXL was measured preoperatively by ultrasonography, and PVD status was classified intraoperatively: broad vitreo-retinal adhesion as no PVD, PVD at the macular area with attachment at the disc as incomplete PVD, and complete PVD. Forty-four eyes had no PVD, 23 had incomplete PVD, and 48 had complete PVD. A majority of the no PVD group had macula off TRD (97.7%), whereas vitreous haemorrhage (68.7%) predominated in the complete PVD group. Longer AXLs were noted in the complete PVD group compared with the no PVD and incomplete PVD groups (ANOVA in three groups P=0.0001). Univariate analysis showed that AXL had an influence on anatomical success (P=0.02). Multiple logistic regression analysis yielded that PVD status is a significant predictor of the final best corrected visual acuity (BCVA)>20/100, and BCVA>20/40 (P=0.01, P=0.02). Intraoperatively assessed PVD status is a prognostic factor for functional outcomes of diabetic vitrectomy. Shorter AXL was associated with lesser PVD. In eyes with a lack of PVD, careful timing and decision of surgery are mandatory.

Insights into the molecular basis of rhegmatogenous retinal detachment

Abstract Purpose Factors that determine the likelihood of developing posterior vitreous detachment and subsequent rhegmatogenous retinal detachment (RRD) include (i) the degree of vitreous liquefaction (ii) the strength of post‐basal vitreoretinal adhesion and (iii) the topology of the posterior border of the vitreous base. The purpose of these studies was to investigate each of these using a combination of ultrastructural and molecular techniques. Methods Ultrastructural studies of the human vitreous and vitreoretinal interface were performed in combination with various antibodies and cationic dyes. Biochemical studies were performed on extracted vitreous components. Results The resultant data suggest that: (i) vitreous liquefaction is caused by the aggregation of vitreous collagen fibrils and this is due to a loss of type IX collagen proteoglycan from the fibril surfaces; (ii) interactions between heparan sulphate proteoglycans in the inner limiting lamina and components on the surface of cortical vitreous collagen fibrils contribute to postbasal vitreoretinal adhesion; (iii) the posterior border of the vitreous base migrates posteriorly with aging due to the synthesis of new vitreous collagen by the peripheral retina. Conclusion The molecular basis of RRD is starting to be unravelled. Furthering our understanding of the underlying molecular processes may lead to the development of novel therapeutic strategies to treat RRD and other vitreoretinal disorders.

PATHOLOGY OF THE MACULAR HOLE RIM IN FLAT-MOUNTED INTERNAL LIMITING MEMBRANE SPECIMENS

The purpose of this study was to image the pathology of vitreoretinal adhesion and cellular proliferation at the macular hole rim for a better understanding of macular hole formation. Internal limiting membrane (ILM) peeling, ILM flat-mount preparation, phase contrast and interference microscopy, transmission electron microscopy, and immunocytochemistry of the macular hole rim were performed in 10 eyes with idiopathic macular holes. Phase contrast and interference microscopy showed cellular proliferation on the vitreal side of the ILM in all specimens. There were single cells in three eyes, cell clusters in six eyes, and continuous proliferation in one eye. Surrounding the macular hole, only a few cells were present. Cellular proliferation started at a distance of 80 mum to 940 mum from the macular hole edge. Transmission electron microscopy showed vitreous adhesion at the macular hole rim. In ultrastructural terms, there was a continuous insertion of vitreous collagen fibers into the ILM. Immunocytochemistry was positive for collagen type II, laminin, and fibronectin in the area of vitreous attachment. Cells were stained with markers for glial cells, retinal pigment epithelial cells, and hyalocytes. There is ultrastructural evidence that macular hole formation is caused by an insertion of the cortical vitreous into the foveal ILM. Vitreous collagen fibers may exert vitreofoveal traction, resulting in a foveal tear. Cellular proliferation is not continuously distributed surrounding the macular hole but separated from the macular hole edge and seems to originate from cell clusters forming centers of proliferation distant from the macular hole rim.

Extrafoveal vitreous traction associated with diabetic diffuse macular oedema

To present an association between diabetic diffuse macular oedema and extrafoveal vitreous traction by optical coherence tomography (OCT). In a retrospective study, charts and OCT scans of diabetic patients with macular oedema were reviewed. Eyes with either vitreofoveal or extrafoveal traction were included. Eyes that had vitreoretinal adherence with no sign of traction, idiopathic vitreomacular traction syndrome, or vitreoretinal surgery were excluded. Macular maps were compared with normal controls (n=12). Of the 186 eyes of 122 consecutive patients, 45 eyes (41 patients) were analyzed. Vitreofoveal traction was detected in 25 eyes (56%) and extrafoveal traction in 20 (44%), either at the retina (16; 35%) or at the optic nerve head (4; 9%). Of these 20 eyes, related extrafoveal retinal oedema was in continuum with the central macular oedema, manifesting as diffuse macular oedema, in 16 (36% of all 45) eyes. Vitreous adherence was detected by the centrally fixated Automatic 6-radial lines program in 26 eyes (58%): 5 (25%) of 20 with extrafoveal traction and 21 (84%) of 25 with vitreofoveal traction. In the other 19 (42%) eyes, the vitreous traction site was detected only by the Line group OCT-2000 program, which is manually controllable during the scanning process. Diabetic diffuse macular oedema may be related to an extrafoveal vitreous traction. The traction sites were detected in a large proportion of eyes only by the OCT Line group program and not by the Automatic 6-radial lines program. Further studies are required to validate the clinical consequence of these findings.

Anatomical findings of vitreoretinal interface in eyes with asteroid hyalosis

To investigate the anatomical features of vitreoretinal interface in eyes with asteroid hyalosis (AH) with optical coherence tomography (OCT) and intravitreal triamcinolone acetonide (TA) during vitreous surgery. This study was an interventional clinical case series. Records relating to ten eyes from ten patients who underwent a TA-assisted vitrectomy for the treatment of diverse vitreoretinal diseases complicated with AH. The posterior vitreoretinal interface was examined by preoperative OCT and by intraoperative visualization of posterior vitreous cortex utilizing TA. In eight of ten AH eyes, preoperative OCT revealed abnormal vitreoretinal adhesions. In four of these eight eyes, posterior vitreoschisis could be seen on OCT. In the other four of these eight eyes, a clear no posterior vitreous detachment (PVD) pattern could be seen on OCT. Although posterior vitreous cortex could not be clearly identified with preoperative OCT in two of ten AH eyes, a complete PVD was refuted by intraoperative visualization of the posterior vitreous cortex with TA identical to the other eight eyes. These results indicate that complete PVD appears to be unlikely to occur in eyes with AH. In addition, spontaneous PVD in eyes with AH might lead to vitreoschisis or residual whole layer or posterior vitreous cortex, possibly due to anomalous vitreoretinal adhesion.

Vitreoretinal Interface Changes in Acute-Onset Postoperative Endophthalmitis

The aim of this study was to assess the significance of different clinical appearances of the vitreoretinal interface in the surgical management of acute postoperative endophthalmitis. 22 patients underwent vitrectomy and were divided intraoperatively in 3 groups according to the degree of vitreoretinal interface changes: 10 patients had white infiltrates in the vitreous cortex but no retinal hemorrhages (group A), eight patients had white infiltrates in the vitreous cortex and retinal hemorrhages (group B) and four patients had advanced vitreous opacification, strong vitreoretinal adhesions and retinal hemorrhages (group C). In group A vitrectomy was performed and the vitreous cortex was removed cautiously, while in groups B and C the vitreous cortex was not removed in the first procedure. Visual acuity improved in 14 patients, remained stable in 2 patients and deteriorated in 6 patients. The visual prognosis was better in group A. None of the cases was complicated with retinal detachment following vitrectomy, but in groups B and C 37.5 % and 50 % of the patients, respectively, went into phthisis. Intraoperative assessment of the vitreoretinal interface insult in acute postoperative endophthalmitis contributes to an optimal surgical management, and it also has a prognostic value.

Comparison of UHR-OCT versus Stratus-OCT for definition of early retinal changes after intravitreal Bevacizumab (Avastin®) application in patients with AMD

PURPOSE: To investigate and demonstrate early structural changes of the retina/pigmentepithelial/choriocapillaris (RPECC) complex before and 10 ± 3 days after intravitreal application of bevacizumab (Avastin®) in patients with neovascular age related macular degeneration (nAMD) by comparison of standard Stratus Optical Coherence Tomography (S-OCT) and Ultra High Resolution (UHR-OCT) imaging systems. METHODS: Six patients with nAMD were examined in a consecutive case series with UHR-OCT and Stratus OCT one day before and 10 ± 3 days after intravitreal application of 1.25 mg (0.125 ml) bevacizumab (Avastin®). Maximum central retinal thickness (CRT) was measured with the retinal thickness program and calliper measuring function of S-OCT and by the measuring tool of Adobe Photoshop 5.0 in UHR-OCT pictures. RESULTS: In three of six cases residual fluid after treatment was only visible with UHR-OCT but not with the S-OCT. A decrease of maximum CRT could be shown in all cases in UHR-OCT pictures but only in half of the cases (6/3) in S-OCT pictures. In 2/6 cases vitreoretinal adhesions were demonstrable with UHR-OCT but not seen with the S-OCT, irregularities in the photoreceptor layer could be revealed clearly by UHR-OCT in 2/6 cases. CONCLUSION: After anti-VEGF treatment, UHR–OCT gives more accurate information about residual fluid and intraretinal damage than S-OCT and offers more precise measurements of maximum CRT. These factors may influence further decision of therapy and give us a better explanation and correlation with unsatisfactory visual acuities than with the S-OCT.

The vitreo-retinal interface in macular diseases

Anomalous posterior vitreous detachment occurs, when the extent of vitreous liquefaction exceeds the degree of weakening of vitreo-retinal adherence and traction is exerted at the vitreo-retinal interface. In the macular region vitreo-macular traction is obviously correlated with macular disorders like macular pucker, epiretinal membrane, macular hole formation, and vitreo-macular traction syndrome. The pathogenesis of diabetic macular edema and exudative age-related macular degeneration is more complex. However, the effectivity of vitrectomy in diabetic macular edema and high incidence of vitreoretinal adhesions in exudative age-related macular degeneration underscore the important role of the vitreous in the pathogenesis of these diseases.