Pars plana vitrectomy combined with internal limiting membrane peeling for recurrent macular edema due to branch retinal vein occlusion after antivascular endothelial growth factor treatments.

PURPOSE: To evaluate the anatomic and functional outcomes of pars plana vitrectomy combined with internal limiting membrane peeling for recurrent macular edema (ME) due to branch retinal vein occlusion (BRVO) after intravitreal injections of antivascular endothelial growth factor (anti-VEGF) agents. METHODS: Twenty-four eyes of 24 patients with treatment-naive ME from BRVO were treated with intravitreal injections of anti-VEGF agents. Recurred ME was treated with pars plana vitrectomy combined with internal limiting membrane peeling. RESULTS: After the surgery, ME was significantly reduced at 1 month (P=0.031) and the reduction increased with time (P=0.007 at the final visit). With the reduction in ME, treated eyes showed a slow improvement in visual acuity (VA). At the final visit, improvement in VA was statistically significant compared with baseline (P=0.048). The initial presence of cystoid spaces, serous retinal detachment, or subretinal hemorrhage under the fovea, as well as retinal perfusion status, showed no association with VA improvement. However, the presence of epiretinal membrane showed a significant association with the visual recovery. Although eyes without epiretinal membrane showed visual improvement (-0.10±0.32 in logarithm of the minimum angle of resolution [logMAR]), eyes with epiretinal membrane showed greater visual improvement (-0.38±0.12 in logMAR, P=0.012). CONCLUSION: For recurrent ME due to BRVO after anti-VEGF treatment, particularly when accompanied by epiretinal membrane, pars plana vitrectomy combined with internal limiting membrane peeling might be a possible treatment option.

A method to decrease the frequency of unintentional slippage after vitrectomy for rhegmatogenous retinal detachment.

PURPOSE: To investigate a method for preventing retinal slippage after standard vitrectomy for rhegmatogenous retinal detachment. METHODS: Eighty six eyes with bullous rhegmatogenous retinal detachment underwent successful standard vitrectomy. Patients were divided into 2 groups. In Group 1, 44 patients started face-down positioning at approximately 10 minutes after the end of the surgery. In Group 2, 42 patients started face-down positioning immediately at the end of the surgery. Postoperative retinal slippage was determined by fundus autofluorescence at 1 month postoperatively. Statistical analysis examined several factors to determine the association between the start time of the face-down positioning and retinal slippage. RESULTS: Retinal slippage occurred in 63.6% of Group 1 and in 24.0% of Group 2 patients. This difference was statistically significant (P = 0.004, Fisher's exact probability test). Both the extent of retinal slippage (P = 0.029) and the face-down position (P < 0.001) were significantly associated with the retinal slippage. CONCLUSION: Earlier implementation of face-down positioning may prevent retinal slippage after surgery in eyes with rhegmatogenous retinal detachment treated by standard vitrectomy.

Displacement of the retina and its recovery after vitrectomy in idiopathic epiretinal membrane.

OBJECTIVE: To study the displacement of the retina and its change after vitrectomy in idiopathic epiretinal membrane (ERM). DESIGN: Prospective, interventional case series. METHODS: Fifty-six eyes of 53 consecutive patients with ERM underwent vitrectomy with ERM removal and internal limiting membrane peeling. Fundus autofluorescence (FAF) imaging was examined before and at 1, 3, 6, and 12 months after vitrectomy. Main outcome measures were the proportion of eyes with retinal displacement for ERM detected by FAF imaging and the recovery rate of retinal displacement after vitrectomy. RESULTS: Before surgery, FAF photography demonstrated hyperautofluorescent lines within the vascular arcade in 37 (66.1%) of the 56 eyes. The lines seemed to be consistent with the location of the retinal vessels before their displacement. These hyperautofluorescent lines appeared significantly more frequently among patients in whom the disease duration was 3 years or less. In 23 (62.2%) of these 37 eyes, within the first postoperative month, the hyperautofluorescent lines disappeared. The disappearance of the hyperautofluorescent line was thought to be the result of the return of the retinal vessel to its original position. Greater visual improvements (logarithm of the minimal angle of resolution, ≥0.3) were statistically significantly obtained in patients in whom the hyperautofluorescent lines had become indistinct at 1 month after surgery (P < .05). CONCLUSIONS: Hyperautofluorescent lines indicating retinal displacement were found by FAF in 66.1% of patients before surgery for ERM. In addition, retinal displacement was significantly more common among patients who had experienced subjective symptoms for 3 years or less. Fundus autofluorescence is useful for predicting postoperative visual acuity improvement.

Correlation of increased fundus autofluorescence signals at closed macula with visual prognosis after successful macular hole surgery.

PURPOSE: To study the significance of the increased fundus autofluorescence (FAF) signals at closed macula with spectral-domain optical coherence tomography and visual prognosis after successful surgery in eyes with idiopathic full-thickness macular holes (MHs). METHODS: Seventy-eight eyes of 78 consecutive patients with full-thickness MHs underwent successful standard vitrectomy, with internal limiting membrane peeling and followed by 10% sulfur hexafluoride gas injection. Simultaneous FAF and optical coherence tomography images were recorded at 10 days, and 1, 3, and 6 months postoperatively, using a combined spectral-domain optical coherence tomography-fluorescein angiography device (Spectralis™/HRA Heidelberg Retina Angiograph 2). The appearance of increased FAF in the macula postoperatively and the relationship of FAF and optical coherence tomography findings to best-corrected visual acuity were examined. RESULTS: Stage 2, 3, and 4 MHs were present in 31, 29, and 18 eyes, respectively. The median patient age was 66 years, with a range of 54 to 79 years. In all patients, the MHs were successfully closed, and the preoperative increased FAF corresponding to MH disappeared 10 days after surgery. In 36 eyes (46.2%), however, hyperautofluorescence again appeared in the macular area 1 month postoperatively. This hyperautofluorescence was significantly associated with the recovery of the external limiting membrane lines at the fovea 1 month after surgery (P = 0.001, multiple logistic regression analysis). Also, this recovery of the external limiting membrane lines 1 month postoperatively was significantly associated with the recovery of photoreceptor inner and outer segment junction line 3 months postoperatively at the fovea (P < 0.001, Fisher exact test). Moreover, a good best-corrected visual acuity of 20/28 or better at 6 months after surgery was significantly associated with hyperautofluorescence in the macula 1 month postoperatively, the recovery of the photoreceptor inner and outer segment lines at the fovea 3 months postoperatively, and preoperative good visual acuity (P < 0.05, multiple logistic regression analysis). CONCLUSION: In full-thickness MHs, 46.2% of our patients showed increased FAF in the macula 1 month after successful MH surgery. This hyperautofluorescence could be a sign of good visual prognosis postoperatively.

[Changes in subfoveal choroidal thickness of epiretinal membrane and macular hole before and after microincision vitrectomy surgery].

PURPOSE: To evaluate the subfoveal choroidal thickness (SCT) of the epiretinal membrane (ERM) and macular hole (MH) both before and after microincision vitrectomy surgery. SUBJECTS AND METHODS: A total of 104 eyes of 104 subjects (64 ERM, 40 MH, mean age 68.9 years) were evaluated. All subjects underwent vitrectomy with internal limiting membrane peeling. SCT was measured before vitrectomy and 1 week, 1 month and 3 months postoperatively. SCT was measured by enhanced depth imaging OCT (EDI-OCT) using a Heiderberg Spectralis. RESULTS: The SCT of ERM was 202.6 microm before vitrectomy, and 201.8 microm at 1 week, 198.8 microm at 1 month, and 196.4 microm at 3 months postoperatively. There were no significant differences between the times of measurement. MH was 182.5 microm before vitrectomy, and 186.7 microm at 1 week, 189.4 microm at 1 month, and 187.4 microm at 3 months. There were also no significant differences between any other factors. The SCT between the ERM and MH was not significantly different at any time. We examined the correlation between the changes in SCT and the changes in age, refractive error and intraocular pressure (IOP), but found no significant correlation. CONCLUSION: The SCT hat not changed either before or after microincision vitrectomy surgery, and there was no siginificant correlation between SCT and any other factor.

Deleterious role of anti-high mobility group box 1 monoclonal antibody in retinal ischemia-reperfusion injury.

PURPOSE: To investigate the effect of anti-high mobility group box 1 (HMGB1) monoclonal antibody (mAb) against ischemia-reperfusion injury in the rat retina. MATERIALS AND METHODS: Retinal ischemia was induced by increasing and then maintaining intraocular pressure at 130 mmHg for 45 min. An intraperitoneal injection of anti-HMGB1 mAb was administered 30 min before ischemia. Retinal damage was evaluated at 7 days after the ischemia. Immunohistochemistry and image analysis were used to measure changes in the levels of reactive oxygen species (ROS) and the localization of anti-HMGB1 mAb. Dark-adapted full-field electroretinography (ERG) was also performed. RESULTS: Pretreatment with anti-HMGB1 mAb significantly enhanced the ischemic injury of the retina. HMGB1 expression increased at 6-12 h after ischemia in the retina. After the ischemia, production of ROS was detected in retinal cells. However, pretreatment with anti-HMGB1 mAb increased the production of ROS. On the seventh postoperative day, the amplitudes of both the ERG a- and b-waves were significantly higher in the vehicle group than in the groups pretreated with anti-HMGB1 mAb. CONCLUSIONS: The current in vivo model of retinal injury demonstrated that anti-HMGB1 mAb plays a large deleterious role in ischemia-reperfusion injury. In order to develop neuroprotective therapeutic strategies for acute retinal ischemic disorders, further studies on anti-HMGB1 mAb function are needed.

D-allose as ischemic retina injury inhibitor during rabbit vitrectomy.

PURPOSE: To investigate the protective effects of D-allose, a rare sugar, on pressure-induced ischemia during vitrectomy in the rabbit eye. METHODS: The rabbits underwent pars plana vitrectomy, and continuous intraocular irrigation at a perfusion pressure of 140 mmHg was performed for 45 min. Intraocular pressure was regulated by adjusting the height of a bottle of balanced saline solution containing D-allose. Morphometric studies were performed to study the effects of D-allose on the histological changes induced by ischemia in the rabbit retina. Electroretinograms (ERGs) were taken before and 1 and 7 days after vitrectomy. Nitroblue tetrazolium was used as an index of superoxide anion (O(2)(·-)) generation. Data were analyzed by use of the unpaired Student's t test. RESULTS: Seven days after ischemia, significant reductions in both number of ganglion cells and the thickness of the inner plexiform layer were observed. D-Allose significantly inhibited ischemic injury of the inner retina (P < 0.05). On postoperative day 7, amplitudes of ERG b-waves were significantly lower in the control group than in the D-allose group (P < 0.05). D-Allose suppressed the production of O(2)(-). CONCLUSIONS: Intraocular irrigation with D-allose during vitrectomy may protect the retina against ischemia-induced damage.

Neuroprotection against retinal ischemia-reperfusion injury by blocking the angiotensin II type 1 receptor.

PURPOSE. To investigate the effects of an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II antagonist against retinal ischemia-reperfusion injury in the rat retina. METHODS. Retinal ischemia was induced by increasing intraocular pressure to 130 mm Hg. Rats were treated with an ACE inhibitor (captopril), an angiotensin II type 1 receptor (AT1-R) antagonist (candesartan), an AT2-R antagonist (PD123319), bradykinin, or a bradykinin B2 receptor antagonist (icatibant). At 7 days after the ischemia, retinal damage was evaluated. Immunohistochemistry and image analysis were used to measure changes in the levels of reactive oxygen species (ROS) and the localization of AT1-R. Dark-adapted full-field electroretinography (ERG) was also performed. RESULTS. Pretreatment with captopril or candesartan significantly inhibited the ischemic injury of the inner retina. However, PD123319, bradykinin, or icatibant did not reduce the ischemic damage. In control retinas, retinal vessels were positive for AT1-R. In contrast, 12 hours after ischemia, immunohistochemical analysis detected numerous AT1-R-positive cells in the inner retina in vehicle-treated rats. After ischemia, the production of ROS was detected in retinal cells. However, pretreatment with captopril or candesartan suppressed the production of ROS. On the seventh postoperative day, the amplitudes of the ERG b-waves were significantly lower in the vehicle group than in the groups pretreated with captopril or candesartan. CONCLUSIONS. The present findings demonstrate that ischemic damage promotes the expression of AT1-R in the inner retina. Both the ACE inhibitor and the AT1-R antagonist that were examined can block the stimulation of the AT1-R and attenuate the subsequent ischemic damage in the rat retina.

Unintentional displacement of the retina after standard vitrectomy for rhegmatogenous retinal detachment.

OBJECTIVE: To study unintentional displacement of the retina after standard vitrectomy for rhegmatogenous retinal detachment (RRD). DESIGN: Prospective interventional case series. PARTICIPANTS: Forty-three eyes of 43 consecutive patients with cystic RRD involving 1 or more quadrants underwent successful standard vitrectomy with 20% sulfur hexafluoride gas injection. Neither scleral buckling nor retinotomy was performed. METHODS: Fundus autofluorescence (FAF) imaging was subsequently recorded to detect displacement of the retina using the Topcon TRC-50DX (Topcon, Tokyo, Japan) at 10 days and 1, 3, and 6 months postoperatively. Fluorescein angiography was also recorded using standard techniques for patients with abnormal FAF findings. Cyclotorsion and vertical deviation were measured postoperatively. MAIN OUTCOME MEASURES: The proportion of eyes with postoperative retinal displacement detected by FAF imaging. RESULTS: The mean age of these 43 patients was 60 years with a range of 39 to 77 years. Of the 43 eyes, retinal detachment involved 1 quadrant in 2 eyes, 2 quadrants in 31 eyes, 3 quadrants in 8 eyes, and 4 quadrants in 2 eyes. After complete reattachment of the retina, FAF photography demonstrated hyperfluorescent lines superiorly parallel to retinal vessels within the vascular arcade in 27 of the 43 eyes (62.8%). Fluorescein angiography did not demonstrate any abnormalities corresponding to the linear autofluorescence. This autofluorescence was hypothesized to originate from increased metabolic activity of the retinal pigment epithelium that had been preoperatively located under the major retinal vessels and was postoperatively exposed to light because of downward displacement of the retina. Of the 27 eyes with retinal displacement, 1 to 5 degrees of extorsion were seen in 16 eyes (59.3%), and 1 to 4 degrees of vertical deviation were seen in 13 eyes (48.1%). None of the 27 patients had diplopia or slant. The extent of retinal detachment (P = 0.019) and the macular status (on or off) (P = 0.016) were significantly associated with postoperative displacement of the retina. CONCLUSIONS: In eyes with RRD treated with standard vitrectomy and gas injection, the retina may move downward after the surgery. If the extent of retinal detachment is large, or macular detachment is present, unintentional postoperative retinal translocation may easily occur. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Neuroprotective effects of angiotensin II type 1 receptor blocker in a rat model of chronic glaucoma.

PURPOSE: To investigate the neuroprotective effect of candesartan, an angiotensin II type 1 receptor (AT1-R) blocker, against the neurotoxicity of the retinal ganglion cells (RGCs) in an animal model of glaucoma. METHODS: Cauterization of three episcleral vessels in rats was used to create chronically elevated intraocular pressure (IOP) in one eye. Rats were then treated orally with candesartan (1 mg/kg/d). At 10 weeks, immunohistochemistry was used for quantification of RGC survival and examination of retinal localization of AT1-R. RESULTS: Compared with the contralateral control eyes, there was a consistently elevated IOP of approximately 2.5-fold during the experimental period. At the end of the 10-week candesartan treatment, there were no changes noted for the blood pressure. Compared with the contralateral control eyes that had normal IOP, the RGC survival rate in the central retina of eyes with the chronic, elevated IOP was 46.5% +/- 19.4% (mean +/- SD) in the untreated animals and 84.2% +/- 4.9% in the candesartan-treated animals (P < 0.05; unpaired t-test). In the retina of the normal IOP rat eyes, retinal vessels were positive for AT1-R. After 10 weeks of IOP elevation, immunohistochemical analysis of the retina indicated there were many AT1-R-positive RGCs in the candesartan-treated rat, whereas there was an apparent AT1-R decrease in the vehicle-treated rats. CONCLUSIONS: In the rat chronic glaucoma model, continuous pharmacologic treatment using candesartan results in significant neuroprotection against RGC loss.